不同灸温调脂通脉效应及TRPV1介导灸法“以温促通”效应机制研究
|
摘要
研究目的：
本课题理论研究部分,通过对古今文献的研究,探讨灸温是影响灸效的关键因素,适宜灸温是取得最佳灸效的重要前提,为下一步灸法“温通”效应机制研究提供理论基础；临床试验部分通过观察不同灸温对高脂血症患者血脂及血清Ox-LDL、ET-1、NO的影响,探讨不同灸温对高脂血症的“温通”效应,观察其能否通过调整血脂组分、抗氧化、保护血管内皮、改善血管舒缩功能、预防AS等不同病理环节体现；动物实验通过观察温度感受器TRPV1的激动剂capsaicin和拮抗剂capsazepine对高脂血症C57BL/6小鼠血脂及背根节TRPV1mRNA表达的影响,从阴性对照和阳性对照两个方面证实TRPV1介导了灸法以“温”促“通”效应机制。
方法：
理论研究：检索与本课题相关的古今文献资料,包括灸温、灸感、灸效、灸法作用机制、高脂血症、TRPV1,综合分析,归纳总结上述资料之间及与本课题之间的相关性,从不同方面为灸法“温通”效应机制研究奠定理论基础。
临床试验：将42例原发性高脂血症患者随机分为45℃组和38℃组,用不同的艾灸温度艾灸患者神阙穴及足三里穴,每次每穴10分钟,隔日一次,治疗12周,肘静脉抽血观察治疗前后患者血脂、血清Ox-LDL、ET-1、NO的变化及组间疗效的差异。
动物实验：分题一,将32只清洁级健康成年雄性C57BL/6小鼠随机分为正常组、模型组、46℃组、38℃组4组,每组8只。自制75%蛋黄乳剂25m1/kg腹腔注射,建立急性高脂血症模型。两次治疗结束后即刻取材,全自动生化分析仪检测血脂,荧光定量PCR法检测小鼠背根节TRPV1mRNA的表达量；分题二,将40只清洁级健康成年雄性C57BL/6小鼠随机分为正常组、模型组、46℃组、46+CPZ组、46+溶媒组5组,每组8只。造模方法同分题一,46+CPZ组在治疗前需涂抹capsazepine,46+溶媒组在治疗前涂抹溶媒剂,其它组处理同分题一,两次治疗结束后即刻取材,检测指标及方法同分题一；分题三,将48只清洁级健康成年雄性C57BL/6小鼠随机分为正常组、模型组、46℃组、38℃组、CAP组、溶媒组6组,每组8只。造模及治疗方法同分题一,CAP组只涂抹capsaicin不治疗,溶媒组只涂抹不治疗,其它组处理同分题一,两次治疗结束后即刻取材,检测指标及方法同分题一。
结果：
临床试验：
1温、热、灼、痛四种不同灸感对应的温度范围有别,“温”的温度范围大概在32.8℃～35.8℃；“热”的温度范围大概在36.8℃～39.9℃；“灼”的温度范围大概在40.9℃～43.5℃；“痛”的温度大概大于等于44.5℃。
2治疗后两组组间比较,45℃组降低了高脂血症患者血清中TC、TG、Ox-LDL的含量及ET-1/NO的比值,明显优于38℃组(P<0.05或者P<0.001)。同时,45℃组升高了高脂血症患者血清中NO的含量,明显优于38℃组(P<0.05)。
345℃和38℃对于血清中Ox-LDL的含量均有明显的降低作用,但38℃组对NO、ET-1、ET-1/NO无明显影响,而45℃组作用明显,说明38℃艾灸对也具有一定的治疗作用,但其作用途径与45℃可能存在着区别。
动物实验：
4与模型组比较,46℃组TC降低明显,差异具有显著性统计学意义(P<0.05),与46℃组比较,38℃组TC含量明显较高,差异具有显著性统计学意义(P<0.05)。46℃组TRPV1mRNA的表达量是模型组的2.62倍,38℃组TRPV1mRNA的表达量是模型组的1.78倍,46℃组TRPV1mRNA的表达量是38℃组的1.47倍。
5与46℃组相比,46+CPZ组TC的含量与明显高于46度组(P<0.05),说明capsazepine拮抗了46℃艾灸的降脂效应。46℃组TRPV1mRNA的表达量是模型组的2.62倍,46+CPZ组TRPV1mRNA的表达量是模型组的1.59倍,说明capsazepine拮抗了46℃艾灸产生的TRPV1mRNA的表达。
6与模型组比较,46℃组、CAP组TC的含量明显降低,且差异有显著统计学意义(P<0.05),CAP组降TC的效应与46℃组降TC的效应从统计学上讲无差异(P>0.05)。46℃组TRPV1mRNA的表达量与CAP组TRPV1mRNA的表达量相同,是模型组的2.62倍,优于38℃组。
理论研究：
7灸感是艾灸起效的关键；温、热、灼、痛是灸感的主要表现形式；适宜的灸量是灸感、灸效产生的重要条件；灸温是不同施灸强度产生的综合灸量,适宜灸温是取得最佳灸效的重要前提。艾灸的作用机理与燃艾时所产生的理化因子有关,如穴位局部感受器、热休克蛋白、肥大细胞脱颗粒等,这些因子都会受到温度的影响,进而产生相应的生物学变化。
结论：
临床研究：
1“温、热、灼、痛”四种不同的灸感对应不同的温度范围,分别是32.8℃～35.8℃.36.8℃～39.9℃.40.9℃～43.5℃.大于等于44.5℃,灸感与温度密切相关。
245℃艾灸刺激具有调脂作用,不同程度地降低了血清中的TC.TG.ApoB.LDL-c的含量,同时明显升高了HDL-C的含量；显著降低了高脂血症患者血清中Ox-LDL的含量,具有抗氧化作用；明显降低了高脂血症患者血清中ET-1含量及降低ET-1/NO比值,同时升高了NO含量,具有保护血管内皮功能作用。
338℃艾灸刺激调脂作用不明显；但可以显著降低高脂血症患者血清中Ox-LDL的含量,具有抗氧化作用；对ET-1、NO的含量及ET-1/NO比值影响不大,保护血管内皮功能作用不明显。
4两组比较,45℃艾灸刺激调脂效应、抗氧化效应及保护血管内皮作用明显较佳。艾灸具有温通调脂作用,“温”是条件,即需达到一定的温度条件,45℃较38℃好,“通”是效应,艾灸刺激达到条件后才会产生较好的调脂通脉效应。
动物研究：
146℃艾灸刺激在降低TC的同时,明显增加了TRPV1mRNA的表达量,不同于38℃。
2局部应用Capsazepine竞争性的拮抗了46℃艾灸热刺激产生的调脂作用,同时也抑制了艾灸热刺激产生的小鼠背根节TRPV1mRNA表达量。
346℃艾灸刺激同Capsaicin一样,均可以激活TRPV1,并产生同样的调脂作用。
4TRPVl介导了灸法以“温”促“通”效应机制,适宜的灸量既要激活TRPV1,同时又可使病人能耐受,即是43℃-45℃。
理论研究：
1灸感是艾灸起效的关键。
2温热灼痛感是灸感的主要表现形式。
3适宜的灸量是灸感、灸效产生的重要条件。
4灸温是不同施灸强度产生的综合灸量,适宜灸温是取得最佳灸效的重要前提。
Objective:
The theoretical study of the subject through the study of ancient and modern literature, investigate that the moxibustion temperature is a key factor to the efficiency of moxibustion, that suitable temperature of the moxibustion is an important prerequisite to obtain the best moxibustion effective, which provide a theoretical basis for the next step moxibustion Warming effect mechanism; Clinical trials through the observation the impact of different moxibustion temperature on the content of lipids and Ox-LDL, ET-1, NO in serum of patients with hyperlipidemia, explore the warming and promoting effect mechanism of moxibustion, to see whether it can be reflect by different aspects of the pathology, including adjusting blood lipid components, antioxidant, protecting vascular endothelial improving vasomotor function, preventing AS and so on.
The animal experiments observed the impact of temperature sensors TRPV1agonist capsaicin and antagonist capsazepine on the blood lipids and TRPV1mRNA expression of dorsal root ganglion in C57BL/6mice with hyperlipidemia. it is confirmed that TRPV1mediated mechanism of moxibustion regulating blood lipids and clearing the blood by negative control study and positive control study.
Method:
Theory research:search related ancient and modern literature, including temperature, feeling, effection, mechanism of moxibustion, hyperlipidemia, TRPV1and then summarize, analysis the correlation between the above information and the this topic.
Method:
Clinical trials:part one:test Li4of20healthy volunteers with laser doppler temperature probe to observe their sense of different temperature; part two:42patients with primary hyperlipidemia were randomly divided into45℃group and38℃, using different temperature moxibustion on CV8and ST36,10minutes for each acupoint one time, every other day at a time, after12weeks of treatment, draw elbow vein blood to observe the changes of index before and after treatment and the curative effect of the differences between groups.
Animal experiment:part one:32SPF level healthy adult male C57BL/6mice were randomly divided into4groups:the normal group, the model group, the46℃group as well as the38℃group, eight for each group. Use selfmade75%egg yolk emulsion as25ml/kg by intraperitoneal injection at one time to foster acute hyperlipidemia model.on9p.m. of the first day, take food away and water left, the next day at13p.m to build mold, after the success of model making, start treatment at the third day. Draw materials immediately on the fourth day after treatment, then detect serum lipids with automatic biochemical analyzer and detect TRPV1mRNA expression amount of dorsal root ganglion by quantitative PCR. part two:40SPF level healthy adult male C57BL/6mice were randomly divided into5groups:46℃group, normal group, model group,46+CPZ group,46+soluble enzyme group, eight for each group.model making and treatment is the same as the part one,46+CPZ group with capsazepine daubed on the acupoints before treatment,46+enzyme group daub soluble enzyme agent before treatment, Draw materials immediately on the fourth day after treatment, then detect serum lipids with automatic biochemical analyzer and detect TRPV1mRNA expression amount of dorsal root ganglion by quantitative PCR; part three,68SPF level healthy adult C57BL/6male mice were randomly divided into6groups, the normal group, model group, the46℃group, the38℃group, the CAP group and the soluble enzyme group, each group of eight mice. Model making and treatment is the same as the part one. The CAP group daub capsaicin without other treatment, as well as the enzyme group. Draw materials immediately on the fourth day after treatment to detect, and then detect serum lipids in mice with automatic biochemical analyzer and detect TRPV1mRNA expression amount of dorsal root ganglion by quantitative PCR.
Result:
Clinical Research:
1there are four moxibustion sense:warm, hot, burning, pain, they have different temperature range, the temperature range of warm is about32.8℃-35.8℃; the temperature range of heat is about36.8℃-39.9℃; the temperature range of hot is about40.9℃-43.5℃; the temperature range of pain is probably greater than or equal to44.5℃。
2Comparison between the two groups after treatment, the45℃group reduce the content of TC, TG, Ox-LDL and ET-1/NO the ratio in the serum of patients with hyperlipidemia, significantly better than the38℃group (P<0.05or P<0.001). In the same time, the45℃group increased the content of NO in the serum of patients with hyperlipidemia, which is significantly better than the38℃group (P<0.05).
3moxibustion stimulate of45℃and38℃can significantly reduce the levels of Ox-LDL in the serum, but the38℃group had no significant impact on the content of NO, ET-1, ET-1/NO, while45℃group had obvious impact. That indicate that moxibustion stimulate of38℃also has a therapeutic effect, but its pathway may be different from45℃moxibustion stimulate.
Experimental Research:
4Compared with the model group, the group of46℃decreased the content of TC significantly(P<0.05); Compared with the46℃group, the content of TC in38℃group is significantly more higher (P<0.05); expression of TRPV1mRNA in the46℃group is2.62times of the model group, the expression of TRPV1mRNA in the38℃group was1.78times of the model group, the amount is38℃group at46℃TRPV1mRNA expression, expression of TRPV1mRNA in the46℃group is1.47times of the38℃group.
5Compared with the46℃group, the content of TC in46+CPZ group is significantly more higher (P<0.05), which indicate that capsazepine antagonized the lipid-lowering effect of46℃group moxibustion. The expression of TRPV1mRNA in the46℃group was2.62times of the model group, The expression of TRPV1mRNA in the46+CPZ group was1.59times of the model groupd, The expression of TRPV1mRNA in the46+CPZ group was1.64times of the46℃groupd, The expression of TRPV1mRNA in the46+soluble enzyme group was2.49times of the model groupd.
6Compared with the model group, the content of TC in46℃group and CAP group was significantly reduced(P<0.05); the CAP group and46℃group statistically speaking had no differences in lowering effect of TC. The expression of TRPV1mRNA in the46℃group was2.62times of the model group. The expression of TRPV1mRNA in the CAP group was2.62times of the model group, the expression of TRPV1mRNA in the38℃group was1.78times of the model group, The expression of TRPV1mRNA in the soluble enzyme group was1.68times of the model groupd.
Theoretical research:
7The moxibustion sense is key in moxibustion onset; warm, hot, burning, pain feeling were the main manifestations of the moxibustion sense; suitable amount of moxibustion was the important condition to get moxibustion sense and the moxibustion efficiency; Moxibustion temperature was comprehensive moxibustion amount of different moxibustion strength, and the suitable moxibustion temperature is an important prerequisite to obtain the best moxibustion effective; moxibustion mechanism is associated with many physical and chemical factors during the action of burning, such as the acupoint local receptors, heat shock proteins, mast cell degranulation, etc, and these factors are affected by temperature and produce biological changes.
Conclusion:
Clinical research:
1warm, hot, buring, pain corespound to four kind of different sense of moxibustion for different temperature range, which is32.8℃to35.8℃,35.8℃to39.9℃,40.9℃to43.5℃, and more than44.5℃. Sense of moxibustion is closely related with temperature.
245℃moxibustion stimulating can regulate the lipid metablison,, reduce the serum TC, TG, ApoB, LDL-c content in different degrees, significantly increase the content of HDL-C;45℃moxibustion stimulation greately reduces the Ox-LDL content in serum of hyperlipidemia patients, proved to have antioxidant effects;45℃moxibustion stimulation can reduce ET-1in serum content, increase NO content and lower ratio of ET-1by NO, hyperlipidemia patients. Thus45℃moxibustion stimulation can protect the vascular endothelial function.
338℃moxibustion stimulation has less effect in regulating the lipid levels;38℃moxibustion stimulation can largely reduce the content of Ox-LDL in serum of hyperlipemia patients, exert antioxidant effects;38℃moxibustion stimulation has little impact on the content of NO and ET-1, ratio of ET-1by NO,which means it can not protect the vascular endothelial function obivosly.
4By contrast,45℃group ofmoxibustion shows better impact on regulating lipid index, exerting antioxidant effect and protecting the vascular endothelial function; moxibustion has the function of warming and promoting to regulate lipid,"warm" is one condition, and it need to reach a certain temperature,45℃is better than38℃,"tong" is the effect of moxibustion stimulation,Only when reaching the certain condition,will it exert better effect of regulating the lipid and unblocking the meridians
Animal studies:
146℃moxibustion stimulation reduced the content of TC, while significantly increase the expression level of TRPV1mRNA, which in different from38℃.
2The local application capsazepine competition antagonised lipid metabolism function of the46℃the moxibustion thermal stimulation, as well as suppress of TRPV1mRNA in the mice dorsal root ganglion induced by moxibustion heat stimuli.
3The same as Capsaicin,46℃moxibustion stimulus can activate TRPV1, and produce the same role in regulate lipid.
4TRPV1mediates moxibustion warming and promoting effect mechanism, and a suitable amount of moxibustion is necessary to activate TRPV1amount. The suitable temperature can enable the patient tolerate and can also activate enough amounts of TRPV1.which is43℃-45℃.
Theoretical studies:
1A moxibustion sense moxibustion onset.
2warm, hot, burning, pain feeling were the main manifestations of the moxibustion sense
3suitable amount of moxibustion was the important condition to get moxibustion sense and the moxibustion efficiency.
4Moxibustion temperature was comprehensive moxibustion amount of different moxibustion strength, and the suitable moxibustion temperature is an important prerequisite to obtain the best moxibustion effective
本课题理论研究部分,通过对古今文献的研究,探讨灸温是影响灸效的关键因素,适宜灸温是取得最佳灸效的重要前提,为下一步灸法“温通”效应机制研究提供理论基础；临床试验部分通过观察不同灸温对高脂血症患者血脂及血清Ox-LDL、ET-1、NO的影响,探讨不同灸温对高脂血症的“温通”效应,观察其能否通过调整血脂组分、抗氧化、保护血管内皮、改善血管舒缩功能、预防AS等不同病理环节体现；动物实验通过观察温度感受器TRPV1的激动剂capsaicin和拮抗剂capsazepine对高脂血症C57BL/6小鼠血脂及背根节TRPV1mRNA表达的影响,从阴性对照和阳性对照两个方面证实TRPV1介导了灸法以“温”促“通”效应机制。
方法：
理论研究：检索与本课题相关的古今文献资料,包括灸温、灸感、灸效、灸法作用机制、高脂血症、TRPV1,综合分析,归纳总结上述资料之间及与本课题之间的相关性,从不同方面为灸法“温通”效应机制研究奠定理论基础。
临床试验：将42例原发性高脂血症患者随机分为45℃组和38℃组,用不同的艾灸温度艾灸患者神阙穴及足三里穴,每次每穴10分钟,隔日一次,治疗12周,肘静脉抽血观察治疗前后患者血脂、血清Ox-LDL、ET-1、NO的变化及组间疗效的差异。
动物实验：分题一,将32只清洁级健康成年雄性C57BL/6小鼠随机分为正常组、模型组、46℃组、38℃组4组,每组8只。自制75%蛋黄乳剂25m1/kg腹腔注射,建立急性高脂血症模型。两次治疗结束后即刻取材,全自动生化分析仪检测血脂,荧光定量PCR法检测小鼠背根节TRPV1mRNA的表达量；分题二,将40只清洁级健康成年雄性C57BL/6小鼠随机分为正常组、模型组、46℃组、46+CPZ组、46+溶媒组5组,每组8只。造模方法同分题一,46+CPZ组在治疗前需涂抹capsazepine,46+溶媒组在治疗前涂抹溶媒剂,其它组处理同分题一,两次治疗结束后即刻取材,检测指标及方法同分题一；分题三,将48只清洁级健康成年雄性C57BL/6小鼠随机分为正常组、模型组、46℃组、38℃组、CAP组、溶媒组6组,每组8只。造模及治疗方法同分题一,CAP组只涂抹capsaicin不治疗,溶媒组只涂抹不治疗,其它组处理同分题一,两次治疗结束后即刻取材,检测指标及方法同分题一。
结果：
临床试验：
1温、热、灼、痛四种不同灸感对应的温度范围有别,“温”的温度范围大概在32.8℃～35.8℃；“热”的温度范围大概在36.8℃～39.9℃；“灼”的温度范围大概在40.9℃～43.5℃；“痛”的温度大概大于等于44.5℃。
2治疗后两组组间比较,45℃组降低了高脂血症患者血清中TC、TG、Ox-LDL的含量及ET-1/NO的比值,明显优于38℃组(P<0.05或者P<0.001)。同时,45℃组升高了高脂血症患者血清中NO的含量,明显优于38℃组(P<0.05)。
345℃和38℃对于血清中Ox-LDL的含量均有明显的降低作用,但38℃组对NO、ET-1、ET-1/NO无明显影响,而45℃组作用明显,说明38℃艾灸对也具有一定的治疗作用,但其作用途径与45℃可能存在着区别。
动物实验：
4与模型组比较,46℃组TC降低明显,差异具有显著性统计学意义(P<0.05),与46℃组比较,38℃组TC含量明显较高,差异具有显著性统计学意义(P<0.05)。46℃组TRPV1mRNA的表达量是模型组的2.62倍,38℃组TRPV1mRNA的表达量是模型组的1.78倍,46℃组TRPV1mRNA的表达量是38℃组的1.47倍。
5与46℃组相比,46+CPZ组TC的含量与明显高于46度组(P<0.05),说明capsazepine拮抗了46℃艾灸的降脂效应。46℃组TRPV1mRNA的表达量是模型组的2.62倍,46+CPZ组TRPV1mRNA的表达量是模型组的1.59倍,说明capsazepine拮抗了46℃艾灸产生的TRPV1mRNA的表达。
6与模型组比较,46℃组、CAP组TC的含量明显降低,且差异有显著统计学意义(P<0.05),CAP组降TC的效应与46℃组降TC的效应从统计学上讲无差异(P>0.05)。46℃组TRPV1mRNA的表达量与CAP组TRPV1mRNA的表达量相同,是模型组的2.62倍,优于38℃组。
理论研究：
7灸感是艾灸起效的关键；温、热、灼、痛是灸感的主要表现形式；适宜的灸量是灸感、灸效产生的重要条件；灸温是不同施灸强度产生的综合灸量,适宜灸温是取得最佳灸效的重要前提。艾灸的作用机理与燃艾时所产生的理化因子有关,如穴位局部感受器、热休克蛋白、肥大细胞脱颗粒等,这些因子都会受到温度的影响,进而产生相应的生物学变化。
结论：
临床研究：
1“温、热、灼、痛”四种不同的灸感对应不同的温度范围,分别是32.8℃～35.8℃.36.8℃～39.9℃.40.9℃～43.5℃.大于等于44.5℃,灸感与温度密切相关。
245℃艾灸刺激具有调脂作用,不同程度地降低了血清中的TC.TG.ApoB.LDL-c的含量,同时明显升高了HDL-C的含量；显著降低了高脂血症患者血清中Ox-LDL的含量,具有抗氧化作用；明显降低了高脂血症患者血清中ET-1含量及降低ET-1/NO比值,同时升高了NO含量,具有保护血管内皮功能作用。
338℃艾灸刺激调脂作用不明显；但可以显著降低高脂血症患者血清中Ox-LDL的含量,具有抗氧化作用；对ET-1、NO的含量及ET-1/NO比值影响不大,保护血管内皮功能作用不明显。
4两组比较,45℃艾灸刺激调脂效应、抗氧化效应及保护血管内皮作用明显较佳。艾灸具有温通调脂作用,“温”是条件,即需达到一定的温度条件,45℃较38℃好,“通”是效应,艾灸刺激达到条件后才会产生较好的调脂通脉效应。
动物研究：
146℃艾灸刺激在降低TC的同时,明显增加了TRPV1mRNA的表达量,不同于38℃。
2局部应用Capsazepine竞争性的拮抗了46℃艾灸热刺激产生的调脂作用,同时也抑制了艾灸热刺激产生的小鼠背根节TRPV1mRNA表达量。
346℃艾灸刺激同Capsaicin一样,均可以激活TRPV1,并产生同样的调脂作用。
4TRPVl介导了灸法以“温”促“通”效应机制,适宜的灸量既要激活TRPV1,同时又可使病人能耐受,即是43℃-45℃。
理论研究：
1灸感是艾灸起效的关键。
2温热灼痛感是灸感的主要表现形式。
3适宜的灸量是灸感、灸效产生的重要条件。
4灸温是不同施灸强度产生的综合灸量,适宜灸温是取得最佳灸效的重要前提。
Objective:
The theoretical study of the subject through the study of ancient and modern literature, investigate that the moxibustion temperature is a key factor to the efficiency of moxibustion, that suitable temperature of the moxibustion is an important prerequisite to obtain the best moxibustion effective, which provide a theoretical basis for the next step moxibustion Warming effect mechanism; Clinical trials through the observation the impact of different moxibustion temperature on the content of lipids and Ox-LDL, ET-1, NO in serum of patients with hyperlipidemia, explore the warming and promoting effect mechanism of moxibustion, to see whether it can be reflect by different aspects of the pathology, including adjusting blood lipid components, antioxidant, protecting vascular endothelial improving vasomotor function, preventing AS and so on.
The animal experiments observed the impact of temperature sensors TRPV1agonist capsaicin and antagonist capsazepine on the blood lipids and TRPV1mRNA expression of dorsal root ganglion in C57BL/6mice with hyperlipidemia. it is confirmed that TRPV1mediated mechanism of moxibustion regulating blood lipids and clearing the blood by negative control study and positive control study.
Method:
Theory research:search related ancient and modern literature, including temperature, feeling, effection, mechanism of moxibustion, hyperlipidemia, TRPV1and then summarize, analysis the correlation between the above information and the this topic.
Method:
Clinical trials:part one:test Li4of20healthy volunteers with laser doppler temperature probe to observe their sense of different temperature; part two:42patients with primary hyperlipidemia were randomly divided into45℃group and38℃, using different temperature moxibustion on CV8and ST36,10minutes for each acupoint one time, every other day at a time, after12weeks of treatment, draw elbow vein blood to observe the changes of index before and after treatment and the curative effect of the differences between groups.
Animal experiment:part one:32SPF level healthy adult male C57BL/6mice were randomly divided into4groups:the normal group, the model group, the46℃group as well as the38℃group, eight for each group. Use selfmade75%egg yolk emulsion as25ml/kg by intraperitoneal injection at one time to foster acute hyperlipidemia model.on9p.m. of the first day, take food away and water left, the next day at13p.m to build mold, after the success of model making, start treatment at the third day. Draw materials immediately on the fourth day after treatment, then detect serum lipids with automatic biochemical analyzer and detect TRPV1mRNA expression amount of dorsal root ganglion by quantitative PCR. part two:40SPF level healthy adult male C57BL/6mice were randomly divided into5groups:46℃group, normal group, model group,46+CPZ group,46+soluble enzyme group, eight for each group.model making and treatment is the same as the part one,46+CPZ group with capsazepine daubed on the acupoints before treatment,46+enzyme group daub soluble enzyme agent before treatment, Draw materials immediately on the fourth day after treatment, then detect serum lipids with automatic biochemical analyzer and detect TRPV1mRNA expression amount of dorsal root ganglion by quantitative PCR; part three,68SPF level healthy adult C57BL/6male mice were randomly divided into6groups, the normal group, model group, the46℃group, the38℃group, the CAP group and the soluble enzyme group, each group of eight mice. Model making and treatment is the same as the part one. The CAP group daub capsaicin without other treatment, as well as the enzyme group. Draw materials immediately on the fourth day after treatment to detect, and then detect serum lipids in mice with automatic biochemical analyzer and detect TRPV1mRNA expression amount of dorsal root ganglion by quantitative PCR.
Result:
Clinical Research:
1there are four moxibustion sense:warm, hot, burning, pain, they have different temperature range, the temperature range of warm is about32.8℃-35.8℃; the temperature range of heat is about36.8℃-39.9℃; the temperature range of hot is about40.9℃-43.5℃; the temperature range of pain is probably greater than or equal to44.5℃。
2Comparison between the two groups after treatment, the45℃group reduce the content of TC, TG, Ox-LDL and ET-1/NO the ratio in the serum of patients with hyperlipidemia, significantly better than the38℃group (P<0.05or P<0.001). In the same time, the45℃group increased the content of NO in the serum of patients with hyperlipidemia, which is significantly better than the38℃group (P<0.05).
3moxibustion stimulate of45℃and38℃can significantly reduce the levels of Ox-LDL in the serum, but the38℃group had no significant impact on the content of NO, ET-1, ET-1/NO, while45℃group had obvious impact. That indicate that moxibustion stimulate of38℃also has a therapeutic effect, but its pathway may be different from45℃moxibustion stimulate.
Experimental Research:
4Compared with the model group, the group of46℃decreased the content of TC significantly(P<0.05); Compared with the46℃group, the content of TC in38℃group is significantly more higher (P<0.05); expression of TRPV1mRNA in the46℃group is2.62times of the model group, the expression of TRPV1mRNA in the38℃group was1.78times of the model group, the amount is38℃group at46℃TRPV1mRNA expression, expression of TRPV1mRNA in the46℃group is1.47times of the38℃group.
5Compared with the46℃group, the content of TC in46+CPZ group is significantly more higher (P<0.05), which indicate that capsazepine antagonized the lipid-lowering effect of46℃group moxibustion. The expression of TRPV1mRNA in the46℃group was2.62times of the model group, The expression of TRPV1mRNA in the46+CPZ group was1.59times of the model groupd, The expression of TRPV1mRNA in the46+CPZ group was1.64times of the46℃groupd, The expression of TRPV1mRNA in the46+soluble enzyme group was2.49times of the model groupd.
6Compared with the model group, the content of TC in46℃group and CAP group was significantly reduced(P<0.05); the CAP group and46℃group statistically speaking had no differences in lowering effect of TC. The expression of TRPV1mRNA in the46℃group was2.62times of the model group. The expression of TRPV1mRNA in the CAP group was2.62times of the model group, the expression of TRPV1mRNA in the38℃group was1.78times of the model group, The expression of TRPV1mRNA in the soluble enzyme group was1.68times of the model groupd.
Theoretical research:
7The moxibustion sense is key in moxibustion onset; warm, hot, burning, pain feeling were the main manifestations of the moxibustion sense; suitable amount of moxibustion was the important condition to get moxibustion sense and the moxibustion efficiency; Moxibustion temperature was comprehensive moxibustion amount of different moxibustion strength, and the suitable moxibustion temperature is an important prerequisite to obtain the best moxibustion effective; moxibustion mechanism is associated with many physical and chemical factors during the action of burning, such as the acupoint local receptors, heat shock proteins, mast cell degranulation, etc, and these factors are affected by temperature and produce biological changes.
Conclusion:
Clinical research:
1warm, hot, buring, pain corespound to four kind of different sense of moxibustion for different temperature range, which is32.8℃to35.8℃,35.8℃to39.9℃,40.9℃to43.5℃, and more than44.5℃. Sense of moxibustion is closely related with temperature.
245℃moxibustion stimulating can regulate the lipid metablison,, reduce the serum TC, TG, ApoB, LDL-c content in different degrees, significantly increase the content of HDL-C;45℃moxibustion stimulation greately reduces the Ox-LDL content in serum of hyperlipidemia patients, proved to have antioxidant effects;45℃moxibustion stimulation can reduce ET-1in serum content, increase NO content and lower ratio of ET-1by NO, hyperlipidemia patients. Thus45℃moxibustion stimulation can protect the vascular endothelial function.
338℃moxibustion stimulation has less effect in regulating the lipid levels;38℃moxibustion stimulation can largely reduce the content of Ox-LDL in serum of hyperlipemia patients, exert antioxidant effects;38℃moxibustion stimulation has little impact on the content of NO and ET-1, ratio of ET-1by NO,which means it can not protect the vascular endothelial function obivosly.
4By contrast,45℃group ofmoxibustion shows better impact on regulating lipid index, exerting antioxidant effect and protecting the vascular endothelial function; moxibustion has the function of warming and promoting to regulate lipid,"warm" is one condition, and it need to reach a certain temperature,45℃is better than38℃,"tong" is the effect of moxibustion stimulation,Only when reaching the certain condition,will it exert better effect of regulating the lipid and unblocking the meridians
Animal studies:
146℃moxibustion stimulation reduced the content of TC, while significantly increase the expression level of TRPV1mRNA, which in different from38℃.
2The local application capsazepine competition antagonised lipid metabolism function of the46℃the moxibustion thermal stimulation, as well as suppress of TRPV1mRNA in the mice dorsal root ganglion induced by moxibustion heat stimuli.
3The same as Capsaicin,46℃moxibustion stimulus can activate TRPV1, and produce the same role in regulate lipid.
4TRPV1mediates moxibustion warming and promoting effect mechanism, and a suitable amount of moxibustion is necessary to activate TRPV1amount. The suitable temperature can enable the patient tolerate and can also activate enough amounts of TRPV1.which is43℃-45℃.
Theoretical studies:
1A moxibustion sense moxibustion onset.
2warm, hot, burning, pain feeling were the main manifestations of the moxibustion sense
3suitable amount of moxibustion was the important condition to get moxibustion sense and the moxibustion efficiency.
4Moxibustion temperature was comprehensive moxibustion amount of different moxibustion strength, and the suitable moxibustion temperature is an important prerequisite to obtain the best moxibustion effective
引文
[1]周嵋生.灸绳[M].山东：青岛出版社,2006：126-130.
[2]陈日新,康明非.腧穴热敏化艾灸新疗法[M].北京：人民卫生出版社,2006：4.
[3]陈日新,陈明人,康明非,等.重视热敏灸感是提高灸疗疗效的关键[J].针刺研究,2010,35(4)：311-314.
[4]陈日新,康明非,何维莉,等.热敏穴灸治疗肌筋膜疼痛综合症：多中心随机对照研究[J].中国针灸,2008,28(6)：395-398.
[5]付勇,康明非,陈日新,等.无痛化脓灸治疗膝关节骨性关节炎疗效观察[J].中国针灸,2007,27(7)：513-515.
[6]章海风,付勇,张波.热敏化灸治疗原发性痛经的临床研究[J].河南中医,2008,28(1)：62-63.
[7]高希言.透灸法及其临床应用[J].河南中医,2007,27(9)：33-34.
[8]刘龙彪,冯祯钰.829例患者灸感观察分析[J].陕西中医,2000,21(4)：176.
[9]杨兆民.刺法灸法学[M].上海：第六版,上海科技出版社出版,2009：78-79.
[10]陈克勤,郝少杰,成新艳,等.灸法循经感传规律的初步研究[J].陕西中医,1988,9(5)：218-220.
[11]刘龙彪,冯祯钰.829例患者灸感观察分析[J].陕西中医,2000,21(4)：176.
[12]洪文学.关于灸疗效果要素的认识与实践[J].中国针灸,2000,(5)：41-42.
[13]李守栋.艾灸的不同刺激量对雷公藤甲素毒副作用的影响[J].甘肃中医,2007,20(1)：49-50.
[14]朱英,芙蕊,陈日兰,等.隔药灸不同灸量对寒凝型痛经患者血清PGF2α/PGE2影响[J].2012,28(4)：606-607.
[15]刘农虞,张蕊,张京英,等.不同灸质、灸量、灸法刺激家兔“足三里”穴对胃电活动的影响[J].针刺研究,1997,22(3)：173-175.
[16]张英,刘又香,孙国杰.不同灸治时程对阳虚小鼠免疫功能影响的比较[J].湖北中医杂志,1998,20
(2)：53-54.
[17]张伟,陈明人,熊俊.不同灸量悬灸“大椎”穴对哮喘大鼠细胞免疫学机制的影响[J].针刺研究,2012,
37(3)：202-205.
[18]嵇明月,王玲玲,姜劲峰,周小云,马明云.温和灸不同灸量对血管内皮功能调节规律的探讨[J].
吉林中医药,2012,32(3)：303-305.
[19]张蕊,刘农虞,张京英.不同灸质、灸量对利血平化大鼠血中组胺与5-羟色胺代谢的影响[J].浙江中
医杂志,1994,(9)：414-415.
[20]张蕊,仇裕丰.不同灸位、刺激量施灸对小鼠耳廓微循环的影响[J].针灸临床杂志,2006,22(9)：46-47.
[21]刘农虞,张京英,张蕊,等.不同灸质、灸量对动物血中5-羟色胺、组织胺含量的影响[J].中国针灸,1995,(5)：29-30.
[22]史曙生.艾灸对运动时血乳酸的影响[J].上海针灸杂志,2002,21(1)：20-21.
[23]顾一煌,金宏柱,吴云川,等.不同艾灸量对运动后血清肌酸激酶影响的实验研究[J].南京中医药大学学报,2006,22(6)：373-375.
[24]顾一煌,任建宁,金宏柱,等.不同的艾灸量对疲劳训练小鼠运动能力的影响[J].陕西中医,2008,29(12)：1686-1687.
[25]顾一煌,金宏柱,吴云川,等.不同的艾灸量对运动后血乳酸影响的观察[J].辽宁中医杂志,2007,34(11)：1639-1640.
[26]张京英,刘农虞,杨兆民,等.不同灸法、灸量对家兔全血组胺含量的影响及其意义[J].中国针灸,1994,14(6)：27-29.
[27]董新民,董泉声,先茂全,等.不同灸法对穴位温度影响的对比观察[J].中国针灸,1999,19(1)：22.
[28]自耀辉,林文任.艾灸与温热刺激关系的探讨[J].针灸学报,1991,(4)：10-11.
[29]董泉声,先茂全,董新民,等.灸法与皮肤感受器的关系[G].四川省中医药研究院临床医学研究所 资料汇编,1995：39.
[30]Dong Q S, Xian M Q, Dong X M, et al. Relation of moxibustion therapy to cutaneous receptors[J].World J Acup-Mox,1998,8(2):32-39.
[31]Dong X M, Dong Q S, Xian M Q, et al. Effect of different moxibustion on the discharge of C polymodal receptors[J]. World J Acup-Mox,1999,9(1):30-39.
[32]Dong Q S, Dong X M, Xian M Q, et al. Antipyreticaction of moxibustion and its relation with acupoint receptors[J]. World J Acup-Mox,2000,10(1):31-35.
[33]Xian M Q, Dong Q S, Zhang S H, et al. Thermolytic effect of moxibustion and its relation to receptors [J]. World J Acup-Mox,2000,10(2):24-31.
[34]董新民,董泉声,张晓琼,等.不同温度灸法的退热作用与体温调节中枢温度敏感神经元活动的关系[J].中国针灸,2012,32(2)：149-154.
[35]kobayashi K. Induntion of heat shock protoin by moxibustion[J].AM.J.Chin.Med.1995,23(34):327-330.
[36]刘旭光,宋开源,郝亮,等.艾灸对实验性RA大鼠热休克蛋白(HSP70)表达的影响[J].中医药学刊,2003,21(7)：1034-1037.
[37]常小荣,彭娜,易受乡,等.艾灸预处理对应激性溃疡大鼠胃薪膜HSP70蛋白及mRNA表达的影响[J].世界华人消化杂志.2006,14(13)：1252-1256.
[38]易受乡,彭艳,常小荣,等.艾灸对应激性胃溃疡大鼠胃粘膜细胞增殖和凋亡的影响及其与热休克蛋白表达关系的研究[J].针刺研究,2006,31(5)：259-271.
[39]常小荣,彭娜,易受乡,等.艾灸足三里和梁门穴诱导热休克蛋白70抗大鼠胃粘膜氧化损伤作用[J].世界华人消化杂志,2006,14(35)：3405-3408.
[40]易受乡,严洁,常小荣,等.艾灸促进胃粘膜细胞HSP70表达上调对细胞凋亡线粒体信号转导途径的影响[J].世界华人消化杂志.2008,16(24)：2689-2694.
[41]郁洁,易受乡,常小荣,等.艾灸足三里、梁门穴对大鼠不同组织器官HSP70表达的影响[J].湖南中医药大学学报,2009,29(4)：67-69.
[42]耿晓英,万琪,杨荣军,等.高温对小鼠神经元骨架蛋白及热休克蛋白70表达的影响[J]第四军医大学学报,2006,27(12)：1090-1091.
[43]耿晓英,吴松笛,万琪.不同温度条件下体外培养小鼠皮质神经元形态及骨架蛋白的表达[J].中国临床康复,2006,10(29)：10-12.
[44]Heib V, Becker M, Taube C, et al. Advances in the understanding of mast cell function[J].Br J Haematol, 2008,142(5):683-694.
[45]张迪,丁光宏,沈学勇,等.经络穴位与肥大细胞相关性研究进展[J].针刺研究,2005,30(2)：115-119.
[46]徐朝霞,郑利岩.经脉与结缔组织相关性研究概况[J].上海针灸杂志,2003,22(3)：45-49.
[47]何俊娜,罗明富.针灸效应与经穴肥大细胞相关性研究概况[J].针刺研究,2007,32(3)：214-216.
[48]罗明富,何俊娜,郭莹,等.电针和悬灸对“大椎”穴区肥大细胞脱颗粒不同影响的研究[J].针刺研究,2007,32(5)：327-329.
[49]刘静,王存诚.生物传热学[M].北京：科学出版社,1997：2-13.
[50]赵镇南.传热学[M].北京：高等教育出版社,2002：8.
[51]洪文学,蔡建红,景军.艾灸的热辐射光谱特性研究[J].应用光学,2004,25(4)：1-3.
[52]洪文学,蔡建红.传统中医艾灸疗法的热辐射光谱特性的研究[J].生物医学工程研究,2003,22(4)：27-30.
[53]杨华元,刘堂义.艾灸疗法的生物物理机制初探[J].中国针灸,1996,16(10)：17.
[54]杨华元,肖元春.隔物灸的近红外光谱辐射特性测定[J].上海针灸杂志,2003,22(19)：15-17.
[55]钟蓝.传统艾灸作用机理初探[J].中国中医基础医学杂志,1999,5(6)：46.
[56]赵吉平译.艾燃烧生成物的自由基清除作用[J].国外医学·中医中药分册,1992,14(3)：60.
[57]黄秋风译.关于艾的燃烧生成物中含有的抗氧化作用物质[J].国外医学·中医中药分册,1989,11(5)： 47.
[58]林文注,王佩.实验针灸学[M].上海：上海科学技术出版社,2005：8.
[59]诸骏仁,陶寿琪.血脂异常防治建议[J].中华心血管杂志,1997,25：169-175.
[60]国家“九五”攻关课题协作组.我国中年人群心血管病主要危险因素流行现状及从80年代初至90年代末的变化趋势[J].中华心血管病杂志,2001,29(2)：66-67.
[61]中国成人血脂异常防治委员会.中国成人血脂异常防治指南(2007年)[J].中华心血管病杂志,2007,35(5)：390-394.
[62]赵冬,吴兆苏,工薇.北京地区1984-1997年急性冠心病事件发病率变化趋势(中国MONICA方案的研究)[J].中华心血管病杂志,2000,28(1)：22-23.
[63]陈小容,聂本刚.阿伐他汀钙对血管性认知障碍合并高脂血症患者的血脂及认知功能的影响[J].中国全科医学,2009,12(15)：1382-1384.
[64]WtZtanJL. Susceptibility of low-density Iipoprotein to oxidative modifieation[J]. AmJMed,1993,94:348.
[65]叶平.血脂的基础与临床[M].北京：人民军医出版社,2002：255-278.
[66]Lamarehe B, Tchemof A, Moorjani S et al.Small dense LDL partiele as a Predictor of the risk of is chemic heart disease in man[J]. Circulation,1997,95:69.
[67]Genest JJ, Jenner JL. Prevalence of Lipoprotein (a) [LP (a)] lexeess in eoronary artery disease[J]. Am J Cardiol,1991,67(12):1039.
[68]Amstrong VM.The assoeiation between LP(a)eoneentrations and angiographically assessed coronary atheroselerosis[J].Atheroselerosis,1989,62(4)-.249.
[69]Pasyk KA, Jakobczak BA.Vascular endothelium:recent advances[J].Eur JDermato,l 2004,14(4) 209-213.
[70]Skultetyova D, Filipova S, Riecansky I, et a.l Endothelial dysfunction and the clinical application[J]. BratislLek Listy,2003,104(1):40-41.
[71]Paterick TE, Fletcher GF. Endothelial function and cardiovascular prevention:role of blood lipids, exercise, and other risk factors[J]. Cardiol Rev,2001,9(5):282-286.
[72]Cai H and Harrison DG. Endothelial dysfunction in cardiovascular diseases:the role of oxidant stress. Circ Res,2000,87:840-844.
[73]Beckman JS and Koppenol WH. Nitric oxide, superoxide, and peroxynitrite:the good, the bad, and ugly. Am J Physiol,1996,271:C1424-C1437.
[74]Groemping Y, Rittinger K. Activation and assembly of the NADPH oxidase:a structural perspective. Biochem J,2005,386:401-416
[75]Lakka HM, Laaksonen DE, Lakka TA, Niskanen LK, Kumpusalo E,Tuomilehto J and Salonen JT. The metabolic syndrome and total and cardiovascular disease mortality in middle-aged men. JAMA,2002, 288:2709-2716.
[76]Sakurai K, Sawamura T. Stress and vascHlar responses:endothelial dysfunction via I ectin like oxidized low density lipoprotein receptor-1:close relationships with oxidative stress[J].J Pharmacol Sci,2003,91(3): 182-186
[77]Mallat Z,Tedgui A. Apoptosis in the vasculature:mechanisms and functional importance[J]. Br J Pharmacol,2000,130(5):947-962.
[78]Geng Y J, Libby P. Progression of atheroma:a struggle between death and procreation[J].Arterioscler Thromb Vasc Biol,2002,22(9):1370-1380.
[79]Coles S M, Maxson J M, Carlson S G, et al. Oxidized LDL-induced injury and apoptosis in atherosclerosis. Potential roles for oxysterols[J]. Trends Cardiovasc Med,2001,11(3/4):131-138.
[80]Napoli C. Oxidation of LDL, atherogenesis, and apoptosis [J]. Ann N Y Acad Sci,2003,1010:698-709.
[81]林丽,唐朝枢,袁文俊.血管内皮的保护策略[J].国外医学生理、病理科学与临床分册,2003,23(4)：334-337.
[82]Berkels R, Stockk lauser K, Rosen R, et al. Current status of platelet nosynthases [J].Thromb Res, 1997,87:51-55.
[83]杨军珂,吴宗贵,郭延松,等.大鼠动脉粥样硬化和高脂血症一氧化氮特点的比较[J].上海医学,2003,26(4)：239-242.
[84]张永珍,闫西艴,张延荣,等.硝苯啶、硫氮卓酮对兔实验性动脉粥样硬化的影响[J].中国病理生理杂志,1992,8(4)：430-434.
[85]Inagami T, Naruse M, Hoover R. Endothelium as an endocrine organ[J]. Annu Rev Physiol,1995,57 (1):171-189.
[86]Masaki T. Possible role of endothelin in endothelial regulation of vascular tone[J] Annu Rev Pharmacol Toxicol 1995,35:235.
[87]Hilal-Dandan R, RamirezMT, Villega S, et al. Endothelin ETA receptor regulates signaling and ANF gene expression via multiple G protein linked pathways[J].Am JPhysio,1 1997,272:130.
[88]王幕一,洪飞,孙桂芝.血栓病的基础与临床[M].沈阳：辽宁科技出版社,1996,132-136.
[89]Folkman J, ShingY. Angiogenesis[J]. J Biol Chem,1992,267:10931-10934.
[90]Felmeden DC, Blann AD, LIP GY Angiogenesis:basic pathophysiology and implications for disease[J]. Eur Heart J.2003,24:586-603.
[91]Bikfalvi A, Bicknell R. Recent advances in angiogenesis, anti-angiogenesis and vascular targeting. Trends Pharmacol Sei,2002,23:576-582.
[92]Wang C Y, Liu P Y, Liao J K. Pleiotropic effects of statin therapy:molecular mechanisms and clinical results [J]. T rends Mol Med,2008,14(1):37-44.
[93]Marcoff L, Thompson P D. The role of coenzyme Q10 instatin-associated myopathy:a systematic review [J]. J Am Coll Cardiol,2007,49(23):2231-2237.
[94]Toth P P. High density lipoprotein as a therapeutic target:clinical evidence and treatment strategies [J]. Am J Cardiol,2005,96 (9A):50K-58K;discu ssion 34K-35K.
[95]Carlson L A. Nicotinic acid:the broad spectrum lipid drug.A 50th anniversary review [J]. J Intern Med, 2005,258(2):94-114.
[96]Shah A, Rader D J, M illar J S. The effect of PPAR-alpha agonismon apolipoprotein metabolism in humans [J]. Atherosclerosis,2010,210(1):5-40.
[97]Jun M, Foote C, Lv J, et al. Effects of fibrates on cardiovascular outcomes:a systematic review andmetaanalysis [J]. Lancet,2010,375(9729):1875-1884.
[98]Turley S D. The role of Niemann Pick C1-Like 1 (NPC1L1) in intestinal sterol absorption [J]. J Clin Lipidol,2008,2(2):S20-S28.
[99]Chiang J Y. Regulation of bile acid synthesis:pathways, nuclearreceptors, and mechanisms [J].J H epatol, 2004,40(3):539-551.
[100]Wierzbicki A S, Hardman T, Prince W T. Future challenges for microsomal transport protein inhibitors [J]. Current Vascular Pharmacology,2009,7(3):277-286.
[101]Meuwese M C, de de Groot E, Duivenvoorden R, et al. ACAT inhibition and progression of carotid atherosclerosis in patients with familial hypercholesterolemia:the CAPTIVATE randomized trial[J]. J Am Med Assoc,2009,301(11):1131-1139.
[102]Buchwald H, Varco R L, Matts J P, et al. Effect of partial ileal bypass surgery on mortality and morbidity from coronary heart disease in patients with hypercholesterolemia. Report of the program on the surgical control of the hyperlipidemias [J]. N Engl J Med,1990,323(14):946-955.
[103]Yokoyama M, Origasa H, Matsuzaki M, et al. Effects of eicosapentaenoic acid on major coronary events in hypercholesterolaemic patients (JELIS):a randomized open-label, blinded endpoint analysis [J]. Lancet, 2007,369(9567):1090-1098.
[104]Barter P J, Caulfield M, Eriksson M, et al. Effects of torcetrapib in patients at high risk for coronary events [J]. N Engl J Med,2007,357 (21):2109-2122.
[105]Simic B, Hermann M, Shaw S Q et al. Torcetrapib impairs endothelial function in hypertension [J]. Eur Heart J,2012,33(13):1615-1624.
[106]徐乃翠,徐晓春,俞琦,等.他汀类药物治疗高脂血症不良反应的观察与护理干预[J].实用医学杂志,2010,26(10)：1834-1836.
[107]Monika L. Depressive symptoms in hypercholesterolemic patients treated with parvastatin[J]. Lancet, 1992,340 (8824):910.
[108]Cuchel Marina, Bloedon LeAnne T, Szapary Philippe,et al. Inhibition of Microsomal Triglyceride Transfer Protein in Familial Hypercholesterolemia[J]. The New England Journal of Medicine,2007,356 (2): 148-156.
[109]Moghadasiam MH, Mancini GB, FrohlichJJ. pharmacotherapy of hypercholesterolemia:Statins in clinical practice[J]. Expertopin pharmacotherapy,2000,1(4):683-695.
[110]刘桂荣,袁汝明.对高脂血症几个问题的探讨[J].山东中医药大学学报,2001,25(5)：33.
[111]叶世龙,刘爱芹.健脾通脉汤治疗高脂血症临床观察[J].中华中医药杂志,2008,23(10)：916-917.
[112]赵林,赵军绩.渗葛降脂宁治疗冠心痛高脂血症疗效观察[J].湖北中医杂志,1999,21(9)：39.
[113]郭姣,朴胜华.从高脂血症发病低龄化趋势探讨其中医发病机制[J].中医药信息,2008,25(6)：4-5.
[114]中国成人血脂异常防治指南制定联合委员会.中国血脂异常防治指南[J].中华心血管杂志,2007,35(5)：390-419.
[115]薛慧,李玉山,谭志鑫.银杏叶茶对高胆固醉饮食小鼠血脂的影响[J].中国现代医学杂志,2001,11(4)：53.
[116]王德山,肖玉芳,许亚杰.枸杞子对老年性高脂血症降脂作用的临床研究[J].辽宁中医杂志,1996,23(10)：475-476.
[117]陶波,帅景贤,吴凤莲.荷叶水煎剂对高脂血症大鼠血脂及血液流变学的影响[J].中医药学报,2000,7(6)：55-56.
[118]张椒英,张旭辉,杏仁油治疗高脂血症疗效观察[J].中医药研究,2002,18(3)：3.
[119]工洪秀.水蛙胶囊治疗高脂血症56例[J].国医论坛,2002,17(5)：62.
[120]周建英,申冬珠.大黄醇提片降脂与抗动脉粥样硬化的研究[J].山东中医药大学学报,1997,21(1)：46-48.
[121]刘智.黄芩茎叶总黄酮治疗2型糖尿病性高脂血症大鼠的实验研究[J].中药新药与临床药理,2009,20(1)：5-6.
[122]滕宇,张秋菊,齐治家.中医药抗脂肪肝的研究进展[J].北京中医药大学学报(中医临床版),2005,12(2)：37-41.
[123]管淑玉,苏薇薇.何首乌的化学成分和药理作用研究进展[J].中南药学,2008,6(4)：454-455.
[124]贺成宏.通络降脂饮治疗高脂血症50例[J].内蒙古中医药,2008(4)：17.
[125]黄敬文,段剑飞,秦书芝.中药治疗高脂血症作用机理研究进展[J].中国现代实用医学杂志,2006,5(8)：30-32.
[126]王帅.从肝论治高脂血症探要[J].实用中医内科杂志,2008,22(9)：40.
[127]赵宝安.理肝清脂饮治疗高脂血症61例[J].湖南中医杂志,2005,21(3)：69-70.
[128]陈辉先.泻肝活血汤治疗高脂血症33例临床观察[J].湖南中医杂志,2008,24(5)：9-11.
[129]吴娅妮.益肝调脂饮治疗高脂血症37例分析[J].中华现代内科学杂志,2007,4(1)：24-25.
[130]陈佑林,常建国.加味胃苓汤治疗脾虚痰湿中阻型高脂血症56例[J].四川中医,2008,26(11)：85.
[131]安凤华,邹德运.健脾化痰通络法治疗高脂血症体会[J].中华临床医学研究杂志,2007,13(4)：530-531.
[132]胡郁坤,李昆三.保和丸加减治疗高脂血症39例临床观察[J].中国中医药杂志,2008,6(5)：18-20.
[133]肖艳皎,刘延祥.试析高脂血症从脾论治[J].医药卫生,2007,36(4)：194.
[134]冯锦.健脾化痰祛湿方治疗高脂血症脾虚痰浊型56例[J].中国中医药科技,2012,19(1)：93.
[135]吴同启.从脾肝论治高脂血症60例[J].陕西中医,2004,25(2)：133-134.
[136]胡元吉,陈庆.疏肝健脾法治疗高脂血症42例[J].中国实验方剂学杂志,2012,18(13)：291-292.
[137]彭小明.丹参首乌山楂饮对血脂代谢紊乱的影响[J].浙江中医杂志,2006：41(7)：413.
[138]刘立.降脂茶治疗高脂血症260例[J].中国中医药信息杂志,2006,13(8)：48-49.
[139]李恩庆,佟晓辉.补肾降脂方治疗高脂血症55例[J].中国中医基础医学杂志,2006,12(3)：212-213.
[140]李进龙,田元祥.杨牧祥治疗高脂血症经验[J].辽宁中医杂志,2008,35(7)：983.
[141]江伟,张惠勤,王秋萍.活血降脂汤对血瘀型高脂血症降脂作用的临床观察与实验研究[J].中国中医基础医学杂志,2008,14(5)：374.
[142]赵秀玲.调脂汤治疗高脂血症的疗效观察[J].四川中医,2006,24(4)：52-53.
[143]刘兰印,信建军.化瘀祛痰饮治疗高脂血症70例临床观察[J].四川中医,2005,23(2)：56.
[144]阿衣努尔·木合买提巴克,陈健.火树华教授治疗高脂血症的中医临床经验[J].新疆中医药,2007,25(4)：89-90.
[145]曾宪国.加味血府逐瘀汤合辛伐他汀治疗高脂血症36例临床观察[J].中医药导报,2011,17(3)：40.
[146]吴中朝,王玲玲,徐兰凤,等.艾灸对高脂血症调脂作用的研究[J].上海针灸杂志,1997,16(6)：5-6.
[147]吴中朝,王玲玲,刘跃光,等.艾灸对老年人血液载脂蛋白研究[J].中国针灸,1998,(5)：261-262.
[148]吴中朝,王玲玲,刘跃光,等.艾灸降血脂作用研究[J].南京中医药大学学报,1996,12(5)：41-42.
[149]常小荣,严洁,易受乡,等.隔药饼灸治疗血脂异常的临床研究[J].中华中医药学刊,2010,28(1)：8-10.
[150]钱小路,鲍春龄,侯文光,等.隔药饼灸治疗更年期综合征合并高血脂疗效观察[J].河北中医,2010,32(10)：79-81.
[151]高耀华,王竹行,陈新黔等.降脂药灸治疗中老年高脂血症的临床研究[J].中国针灸,2000,(2)：77-78.
[152]邓柏颖,谢感共,罗本华等.功能保健灸治疗高脂血症40例疗效观察[J].新中医,2002,34(9)：48-49.
[153]王国明,沈玲哲,温峰云,等.瘢痕灸治疗高脂血症40例临床观察[J].中国中医药信息杂志,2000,
7(11)：72-73.
[154]李建萍,姚永年,何培达等.艾灸治疗血脂异常患者的临床研究[J].中国针灸,2005,25(11)：825-827.
[155]吴中朝,刘跃光,王玲玲,等.艾灸抗高甘油三酯血症脂质过氧化正交试验临床研究[J].中国针灸,1998(6)：325-327.
[156]牛晓红,金红,宋剑南等.灸神阙降脂抗氧化作用的研究[J].中国中医基础医学杂志,2003,9(10)：71-77.
[157]岳增辉,严洁,常小荣,等.隔药饼灸对高脂血症兔主动脉内皮细胞超微结构的影响[J].中国针灸,2005,25(1)：64-67.
[158]常小荣,严洁,岳增辉,等.隔药饼灸对高脂血症兔血浆ET、NO含量的影响[J].中国中医药信息杂志,2005,12(6)：20-21.
[159]沈菁,常小荣,严洁,等.隔药饼灸对高脂血症兔血浆内皮素及一氧化氮含量的调节[J].中国临床康复,2006,10(27)：184-186
[160]岳增辉,常小荣,严洁,等.隔药饼灸对兔高脂血症合并动脉粥样硬化主动脉血管细胞黏附分子-1mRNA表达的影响[J].针刺研究,2006,31(3)：145-148.
[161]岳增辉,严洁,常小荣,等.隔药饼灸对兔高脂血症合并动脉粥样硬化血管内皮细胞黏附因子E选择素mRNA表达的影响[J].中国针灸,2006,13(7)：37-39.
[162]常小荣,严洁,岳增辉,等.隔药饼灸对高脂血症兔血浆前列环素和血栓素含量的影响[J].中国临 床康复,2008,8(33)：7446-7447.
[163]吴中朝,刘跃光,王玲玲,等HTG艾灸降脂正交设计研究[J].南京中医药大学学报,1998,14(5)：291.
[164]李爱军.隔药饼灸治疗高脂血症的临床研究[J].广西中医药,2007,30(3)：12-13.
[165]Caterina M J, Schumacher MA, Tominaga M, et al. The capsaicin receptor:a heat-activated ion channel in the pain pathway. Nature,1997,389:816-824.
[166]Venkataehalam K, Monteil C. TRP Channels[J].Annu Rev Biochem,2007,76:387-417.
[167]Luo Z, Ma L, Zhao Z, et al. TRPV1 activation improves exercise endurance and energy metabolism through PGC-1 alpha upregulation in mice[J]. Cell Research,2012,22(3):551-564.
[168]Tousova K, Susankova K, Teisinger J, et al. Oxidizing reagent copper-o-phenanthroline is an open channel blocker of the vanilloid receptor TRPVl[J]. Neuropharmacology,2004,47:273-285.
[169]Clapham DE. Snapshot:mammalian TRP channels[J]. Cell,2007,129:220.
[170]Firth AL, Remillard CV, Yuan JX. TRP channels in hypertension[J]. Biochim Biophys Acta,2007,1772: 895-906.
[171]Tousova K, Susankova K, Teisinger J, et al. Oxidizing reagent copperophenanthroline is an open channel blocker of the vanilloid receptor TRPV1[J]. Neuropharmacology,2004,47:273-285.
[172]Ramsey IS, Delling M, Clapham DE. An introduction to TRP channels[J]. Annu Rev Physiol,2006,68: 619-47.
[173]Mandadi S, Tominaga T, Numazaki M, et al. Increased sensitivity of desensitized TRP V1 by PMA occurs through PKCepsilon-mediated phosphory lationatS800[J].Pain,2006,123(1-2):106-16.
[174]ALAWI K, KEEBLE J. The paradoxical role of the transient receptor potential vanilloid 1 receptor in inflammation[J]. Pharmacol Ther,2010,125(2):181-195.
[175]Pandolfi A, Grilli A, Cilli C, et al. Phenotype modulation in cultures of vascular smooth muscle cells from diabetic rats:association with increased nitric oxide synthase expression and superoxide anion generation[J]. J Cell Physiol,2003,196:378-385.
[176]Gunthorpe MJ, Szallasi A. Peripheral TRPV1 receptors as targets for drug development:new molecules and mechanisms[J]. Curr Pharm Des,2008,14:32-41.
[177]Yang XR, Lin MJ, McIntosh LS, et al. Functional expression of transient receptor potential melastatin-and vanilloid-related channels in pulmonary arterial and aortic smooth muscle[J]. Am J Physiol Lung Cell Mol Physiol,2006,290:L1267-1276.
[178]Ma L, Zhong J, Zhao Z, et al. Activation of TRPV1 reduces vascular lipid accumulation and attenuates atherosclerosis[J]. Cardiovasc Res,2011,92(3):504-513.
[179]Bratz I N, Dick G M, Tune J D, et al. Impaired capsaicin-induced relaxation of coronary arteries in a porcine model of the metabolic syndrome[J]. Am J Physiol Heart Circ Physiol,2008,294(6):H2489-2496.
[180]Zhang L L, Yan Liu D, Ma L Q, et al. Activation of transient receptor potential vanilloid type-1 channel prevents adipogenesis and obesity [J]. Circ Res,2007,100(7):1063-1070.
[181]Hwang SW, Cho H, Kwak J, et al. Direct activation of capsaicin receptors by products of lipoxygenases: endogenous capsaicin-like substances. Proc Natl Acad Sci U S A 2000,97:6155-6160.
[182]Zygmunt PM, Petersson J, Andersson DA, Chuang H, Sorgard M, Di Marzo V, et al.Vanilloid receptors on sensory nerves mediate the vasodilator action of anandamide. Nature,1999,400:452-457.
[183]Yoshida T, Inoue R, Morii T, Takahashi N, Yamamoto S, Hara Y, et al. Nitric oxide activates TRP channels by cysteine S-nitrosylation[J]. Nat Chem Biol,2006,2:596-607.
[184]Cheng W, rang F, Takanishi CL, et al. Thermosensitive TRPV channel subunits coassemble into heteromeric channels with intermediate conductance and gating properties[J]. J Gen Physiol,2007,129(3): 191-207.
[185]Baylie R L, Brayden J E. TRPV channels and vascular function[J]. ActaPhysiologica,2011,203 (1):99-116.
[186]Yang D, Luo Z, Ma S, et al. Activation of TRPV1 by Dietary Capsaicin Improves Endothelium Dependent Vasorelaxation and Prevents Hypertension[J]. Cell Metab,2010,12(2):130-141
[187]Poblete I M, Orliac M L, Briones R, et al. Anandamide elicits an acute release of nitric oxide through endothelial TRPV1 receptor activation in the rat arterial mesenteric bed[J]. The Journal of physiology,2005, 568(2):539-551.
[188]Huang W, Wang H, Galligan JJ, et al. Transient recept or pot entail vanilloid subtype 1 channel mediated neuropeptide secretion and depressor effects:role of endoplasmic reticulum associated Ca2+ release receptors in rat dorsal root ganglion neurons[J]. J Hypertens,2008,26(10):1966-1975.
[189]Ahuja, K. D.; Ball, M. J. Effects of daily ingestion of chilli on serum lipoprotein oxidation in adult men and women[J]. The British journal of nutrition,2006,96(2):239-242.
[190]Ahuja K D, Kunde D A, Ball M J, et al. Effects of capsaicin, dihydrocapsaicin, and curcumin on copper-induced oxidation of human serum lipids[J]. J Agric Food Chem,2006,54(17):6436-6439.
[191]Rosa A, Appendino G, Melis M P, et al. Protective effect and relation structure-activity of nonivamide and iododerivatives in several models of lipid oxidation[J]. Chemico-Biological Interactions,2009,180(2): 183-192.
[192]Ohnuki K, Haramizu S, Oki K, et al. Administration of capsiate, a non-pungent capsaicin analog, promotes energy metabolism and suppresses body fat accumulation in mice[J]. Bioscience, biotechnology, and biochemistry,2001,65(12):2735-2740.
[193]Yoshioka M, St-Pierre S, Suzuki M, et al. Effects of red pepper added to high-fat and high-carbohydrate meals on energy metabolism and substrate utilization in Japanese women[J]. The British journal of nutrition, 1998,80(6):503-510.
[194]Zhang LL, Liu DY, Ma LQ, et al. Activation of transient receptor potential vanilloid type-1 channel prevents adipogenesis and obesity [J].Circ Res,2007,100(7):1063-1070.
[195]Manjunatha H, Srinivasan K. Hypolipidemic and ant ioxidant effects of curcumin and capsaicin in high-fat-fed rats[J]. Can J Physiol Pharmacol,2007,85(6):588-596.
[196]GUNTHORPE MJ, SZALLASI A. Peripheral TRPV1 receptors as targets for drug development:new molecules and mechanisms[J]. Curr Pharm Des,2008,14(1):32-41.
[197]Puntambekar P, Van Buren J, Raisinghani M, et al. Direct interaction of adenosine with the TRPV1 channel protein[J]. J Neurosci,2004,24:3663-3667.
[198]杨莉,李亮,朱兵,等.灸法疗效主要影响因素的分析研究[J].世界中医药,2009,4(4)：217-219.
[199]王玲玲.艾灸的特点及温通效应[J].中国针灸,2011,31(10)：865-868.
[200]中国成人血脂异常防治指南制订委员会.中国成人血脂异常防治指南[J].中华心血管杂志,2007,35(5)：390-419.
[201]Cesare P, Moriondo A, VellaniV, et al. Ion channels gated by heat[J]. Proc Natl Acad Sci,1999,96: 765-766.
[202]刘凯,李传富,申冬珠.大鼠高胆固醇血症快速造型法初筛降脂中草药[J].徐州医学院学报,1990,10(4)：260-262.
[203]王乐,王兰兰,曹宇.TRPV1对LPS致热大鼠体温及下丘脑中Ca2+浓度和cAMP含量的影响[J].中国药理学通报,2009,25(1)：51-55.
[2]陈日新,康明非.腧穴热敏化艾灸新疗法[M].北京：人民卫生出版社,2006：4.
[3]陈日新,陈明人,康明非,等.重视热敏灸感是提高灸疗疗效的关键[J].针刺研究,2010,35(4)：311-314.
[4]陈日新,康明非,何维莉,等.热敏穴灸治疗肌筋膜疼痛综合症：多中心随机对照研究[J].中国针灸,2008,28(6)：395-398.
[5]付勇,康明非,陈日新,等.无痛化脓灸治疗膝关节骨性关节炎疗效观察[J].中国针灸,2007,27(7)：513-515.
[6]章海风,付勇,张波.热敏化灸治疗原发性痛经的临床研究[J].河南中医,2008,28(1)：62-63.
[7]高希言.透灸法及其临床应用[J].河南中医,2007,27(9)：33-34.
[8]刘龙彪,冯祯钰.829例患者灸感观察分析[J].陕西中医,2000,21(4)：176.
[9]杨兆民.刺法灸法学[M].上海：第六版,上海科技出版社出版,2009：78-79.
[10]陈克勤,郝少杰,成新艳,等.灸法循经感传规律的初步研究[J].陕西中医,1988,9(5)：218-220.
[11]刘龙彪,冯祯钰.829例患者灸感观察分析[J].陕西中医,2000,21(4)：176.
[12]洪文学.关于灸疗效果要素的认识与实践[J].中国针灸,2000,(5)：41-42.
[13]李守栋.艾灸的不同刺激量对雷公藤甲素毒副作用的影响[J].甘肃中医,2007,20(1)：49-50.
[14]朱英,芙蕊,陈日兰,等.隔药灸不同灸量对寒凝型痛经患者血清PGF2α/PGE2影响[J].2012,28(4)：606-607.
[15]刘农虞,张蕊,张京英,等.不同灸质、灸量、灸法刺激家兔“足三里”穴对胃电活动的影响[J].针刺研究,1997,22(3)：173-175.
[16]张英,刘又香,孙国杰.不同灸治时程对阳虚小鼠免疫功能影响的比较[J].湖北中医杂志,1998,20
(2)：53-54.
[17]张伟,陈明人,熊俊.不同灸量悬灸“大椎”穴对哮喘大鼠细胞免疫学机制的影响[J].针刺研究,2012,
37(3)：202-205.
[18]嵇明月,王玲玲,姜劲峰,周小云,马明云.温和灸不同灸量对血管内皮功能调节规律的探讨[J].
吉林中医药,2012,32(3)：303-305.
[19]张蕊,刘农虞,张京英.不同灸质、灸量对利血平化大鼠血中组胺与5-羟色胺代谢的影响[J].浙江中
医杂志,1994,(9)：414-415.
[20]张蕊,仇裕丰.不同灸位、刺激量施灸对小鼠耳廓微循环的影响[J].针灸临床杂志,2006,22(9)：46-47.
[21]刘农虞,张京英,张蕊,等.不同灸质、灸量对动物血中5-羟色胺、组织胺含量的影响[J].中国针灸,1995,(5)：29-30.
[22]史曙生.艾灸对运动时血乳酸的影响[J].上海针灸杂志,2002,21(1)：20-21.
[23]顾一煌,金宏柱,吴云川,等.不同艾灸量对运动后血清肌酸激酶影响的实验研究[J].南京中医药大学学报,2006,22(6)：373-375.
[24]顾一煌,任建宁,金宏柱,等.不同的艾灸量对疲劳训练小鼠运动能力的影响[J].陕西中医,2008,29(12)：1686-1687.
[25]顾一煌,金宏柱,吴云川,等.不同的艾灸量对运动后血乳酸影响的观察[J].辽宁中医杂志,2007,34(11)：1639-1640.
[26]张京英,刘农虞,杨兆民,等.不同灸法、灸量对家兔全血组胺含量的影响及其意义[J].中国针灸,1994,14(6)：27-29.
[27]董新民,董泉声,先茂全,等.不同灸法对穴位温度影响的对比观察[J].中国针灸,1999,19(1)：22.
[28]自耀辉,林文任.艾灸与温热刺激关系的探讨[J].针灸学报,1991,(4)：10-11.
[29]董泉声,先茂全,董新民,等.灸法与皮肤感受器的关系[G].四川省中医药研究院临床医学研究所 资料汇编,1995：39.
[30]Dong Q S, Xian M Q, Dong X M, et al. Relation of moxibustion therapy to cutaneous receptors[J].World J Acup-Mox,1998,8(2):32-39.
[31]Dong X M, Dong Q S, Xian M Q, et al. Effect of different moxibustion on the discharge of C polymodal receptors[J]. World J Acup-Mox,1999,9(1):30-39.
[32]Dong Q S, Dong X M, Xian M Q, et al. Antipyreticaction of moxibustion and its relation with acupoint receptors[J]. World J Acup-Mox,2000,10(1):31-35.
[33]Xian M Q, Dong Q S, Zhang S H, et al. Thermolytic effect of moxibustion and its relation to receptors [J]. World J Acup-Mox,2000,10(2):24-31.
[34]董新民,董泉声,张晓琼,等.不同温度灸法的退热作用与体温调节中枢温度敏感神经元活动的关系[J].中国针灸,2012,32(2)：149-154.
[35]kobayashi K. Induntion of heat shock protoin by moxibustion[J].AM.J.Chin.Med.1995,23(34):327-330.
[36]刘旭光,宋开源,郝亮,等.艾灸对实验性RA大鼠热休克蛋白(HSP70)表达的影响[J].中医药学刊,2003,21(7)：1034-1037.
[37]常小荣,彭娜,易受乡,等.艾灸预处理对应激性溃疡大鼠胃薪膜HSP70蛋白及mRNA表达的影响[J].世界华人消化杂志.2006,14(13)：1252-1256.
[38]易受乡,彭艳,常小荣,等.艾灸对应激性胃溃疡大鼠胃粘膜细胞增殖和凋亡的影响及其与热休克蛋白表达关系的研究[J].针刺研究,2006,31(5)：259-271.
[39]常小荣,彭娜,易受乡,等.艾灸足三里和梁门穴诱导热休克蛋白70抗大鼠胃粘膜氧化损伤作用[J].世界华人消化杂志,2006,14(35)：3405-3408.
[40]易受乡,严洁,常小荣,等.艾灸促进胃粘膜细胞HSP70表达上调对细胞凋亡线粒体信号转导途径的影响[J].世界华人消化杂志.2008,16(24)：2689-2694.
[41]郁洁,易受乡,常小荣,等.艾灸足三里、梁门穴对大鼠不同组织器官HSP70表达的影响[J].湖南中医药大学学报,2009,29(4)：67-69.
[42]耿晓英,万琪,杨荣军,等.高温对小鼠神经元骨架蛋白及热休克蛋白70表达的影响[J]第四军医大学学报,2006,27(12)：1090-1091.
[43]耿晓英,吴松笛,万琪.不同温度条件下体外培养小鼠皮质神经元形态及骨架蛋白的表达[J].中国临床康复,2006,10(29)：10-12.
[44]Heib V, Becker M, Taube C, et al. Advances in the understanding of mast cell function[J].Br J Haematol, 2008,142(5):683-694.
[45]张迪,丁光宏,沈学勇,等.经络穴位与肥大细胞相关性研究进展[J].针刺研究,2005,30(2)：115-119.
[46]徐朝霞,郑利岩.经脉与结缔组织相关性研究概况[J].上海针灸杂志,2003,22(3)：45-49.
[47]何俊娜,罗明富.针灸效应与经穴肥大细胞相关性研究概况[J].针刺研究,2007,32(3)：214-216.
[48]罗明富,何俊娜,郭莹,等.电针和悬灸对“大椎”穴区肥大细胞脱颗粒不同影响的研究[J].针刺研究,2007,32(5)：327-329.
[49]刘静,王存诚.生物传热学[M].北京：科学出版社,1997：2-13.
[50]赵镇南.传热学[M].北京：高等教育出版社,2002：8.
[51]洪文学,蔡建红,景军.艾灸的热辐射光谱特性研究[J].应用光学,2004,25(4)：1-3.
[52]洪文学,蔡建红.传统中医艾灸疗法的热辐射光谱特性的研究[J].生物医学工程研究,2003,22(4)：27-30.
[53]杨华元,刘堂义.艾灸疗法的生物物理机制初探[J].中国针灸,1996,16(10)：17.
[54]杨华元,肖元春.隔物灸的近红外光谱辐射特性测定[J].上海针灸杂志,2003,22(19)：15-17.
[55]钟蓝.传统艾灸作用机理初探[J].中国中医基础医学杂志,1999,5(6)：46.
[56]赵吉平译.艾燃烧生成物的自由基清除作用[J].国外医学·中医中药分册,1992,14(3)：60.
[57]黄秋风译.关于艾的燃烧生成物中含有的抗氧化作用物质[J].国外医学·中医中药分册,1989,11(5)： 47.
[58]林文注,王佩.实验针灸学[M].上海：上海科学技术出版社,2005：8.
[59]诸骏仁,陶寿琪.血脂异常防治建议[J].中华心血管杂志,1997,25：169-175.
[60]国家“九五”攻关课题协作组.我国中年人群心血管病主要危险因素流行现状及从80年代初至90年代末的变化趋势[J].中华心血管病杂志,2001,29(2)：66-67.
[61]中国成人血脂异常防治委员会.中国成人血脂异常防治指南(2007年)[J].中华心血管病杂志,2007,35(5)：390-394.
[62]赵冬,吴兆苏,工薇.北京地区1984-1997年急性冠心病事件发病率变化趋势(中国MONICA方案的研究)[J].中华心血管病杂志,2000,28(1)：22-23.
[63]陈小容,聂本刚.阿伐他汀钙对血管性认知障碍合并高脂血症患者的血脂及认知功能的影响[J].中国全科医学,2009,12(15)：1382-1384.
[64]WtZtanJL. Susceptibility of low-density Iipoprotein to oxidative modifieation[J]. AmJMed,1993,94:348.
[65]叶平.血脂的基础与临床[M].北京：人民军医出版社,2002：255-278.
[66]Lamarehe B, Tchemof A, Moorjani S et al.Small dense LDL partiele as a Predictor of the risk of is chemic heart disease in man[J]. Circulation,1997,95:69.
[67]Genest JJ, Jenner JL. Prevalence of Lipoprotein (a) [LP (a)] lexeess in eoronary artery disease[J]. Am J Cardiol,1991,67(12):1039.
[68]Amstrong VM.The assoeiation between LP(a)eoneentrations and angiographically assessed coronary atheroselerosis[J].Atheroselerosis,1989,62(4)-.249.
[69]Pasyk KA, Jakobczak BA.Vascular endothelium:recent advances[J].Eur JDermato,l 2004,14(4) 209-213.
[70]Skultetyova D, Filipova S, Riecansky I, et a.l Endothelial dysfunction and the clinical application[J]. BratislLek Listy,2003,104(1):40-41.
[71]Paterick TE, Fletcher GF. Endothelial function and cardiovascular prevention:role of blood lipids, exercise, and other risk factors[J]. Cardiol Rev,2001,9(5):282-286.
[72]Cai H and Harrison DG. Endothelial dysfunction in cardiovascular diseases:the role of oxidant stress. Circ Res,2000,87:840-844.
[73]Beckman JS and Koppenol WH. Nitric oxide, superoxide, and peroxynitrite:the good, the bad, and ugly. Am J Physiol,1996,271:C1424-C1437.
[74]Groemping Y, Rittinger K. Activation and assembly of the NADPH oxidase:a structural perspective. Biochem J,2005,386:401-416
[75]Lakka HM, Laaksonen DE, Lakka TA, Niskanen LK, Kumpusalo E,Tuomilehto J and Salonen JT. The metabolic syndrome and total and cardiovascular disease mortality in middle-aged men. JAMA,2002, 288:2709-2716.
[76]Sakurai K, Sawamura T. Stress and vascHlar responses:endothelial dysfunction via I ectin like oxidized low density lipoprotein receptor-1:close relationships with oxidative stress[J].J Pharmacol Sci,2003,91(3): 182-186
[77]Mallat Z,Tedgui A. Apoptosis in the vasculature:mechanisms and functional importance[J]. Br J Pharmacol,2000,130(5):947-962.
[78]Geng Y J, Libby P. Progression of atheroma:a struggle between death and procreation[J].Arterioscler Thromb Vasc Biol,2002,22(9):1370-1380.
[79]Coles S M, Maxson J M, Carlson S G, et al. Oxidized LDL-induced injury and apoptosis in atherosclerosis. Potential roles for oxysterols[J]. Trends Cardiovasc Med,2001,11(3/4):131-138.
[80]Napoli C. Oxidation of LDL, atherogenesis, and apoptosis [J]. Ann N Y Acad Sci,2003,1010:698-709.
[81]林丽,唐朝枢,袁文俊.血管内皮的保护策略[J].国外医学生理、病理科学与临床分册,2003,23(4)：334-337.
[82]Berkels R, Stockk lauser K, Rosen R, et al. Current status of platelet nosynthases [J].Thromb Res, 1997,87:51-55.
[83]杨军珂,吴宗贵,郭延松,等.大鼠动脉粥样硬化和高脂血症一氧化氮特点的比较[J].上海医学,2003,26(4)：239-242.
[84]张永珍,闫西艴,张延荣,等.硝苯啶、硫氮卓酮对兔实验性动脉粥样硬化的影响[J].中国病理生理杂志,1992,8(4)：430-434.
[85]Inagami T, Naruse M, Hoover R. Endothelium as an endocrine organ[J]. Annu Rev Physiol,1995,57 (1):171-189.
[86]Masaki T. Possible role of endothelin in endothelial regulation of vascular tone[J] Annu Rev Pharmacol Toxicol 1995,35:235.
[87]Hilal-Dandan R, RamirezMT, Villega S, et al. Endothelin ETA receptor regulates signaling and ANF gene expression via multiple G protein linked pathways[J].Am JPhysio,1 1997,272:130.
[88]王幕一,洪飞,孙桂芝.血栓病的基础与临床[M].沈阳：辽宁科技出版社,1996,132-136.
[89]Folkman J, ShingY. Angiogenesis[J]. J Biol Chem,1992,267:10931-10934.
[90]Felmeden DC, Blann AD, LIP GY Angiogenesis:basic pathophysiology and implications for disease[J]. Eur Heart J.2003,24:586-603.
[91]Bikfalvi A, Bicknell R. Recent advances in angiogenesis, anti-angiogenesis and vascular targeting. Trends Pharmacol Sei,2002,23:576-582.
[92]Wang C Y, Liu P Y, Liao J K. Pleiotropic effects of statin therapy:molecular mechanisms and clinical results [J]. T rends Mol Med,2008,14(1):37-44.
[93]Marcoff L, Thompson P D. The role of coenzyme Q10 instatin-associated myopathy:a systematic review [J]. J Am Coll Cardiol,2007,49(23):2231-2237.
[94]Toth P P. High density lipoprotein as a therapeutic target:clinical evidence and treatment strategies [J]. Am J Cardiol,2005,96 (9A):50K-58K;discu ssion 34K-35K.
[95]Carlson L A. Nicotinic acid:the broad spectrum lipid drug.A 50th anniversary review [J]. J Intern Med, 2005,258(2):94-114.
[96]Shah A, Rader D J, M illar J S. The effect of PPAR-alpha agonismon apolipoprotein metabolism in humans [J]. Atherosclerosis,2010,210(1):5-40.
[97]Jun M, Foote C, Lv J, et al. Effects of fibrates on cardiovascular outcomes:a systematic review andmetaanalysis [J]. Lancet,2010,375(9729):1875-1884.
[98]Turley S D. The role of Niemann Pick C1-Like 1 (NPC1L1) in intestinal sterol absorption [J]. J Clin Lipidol,2008,2(2):S20-S28.
[99]Chiang J Y. Regulation of bile acid synthesis:pathways, nuclearreceptors, and mechanisms [J].J H epatol, 2004,40(3):539-551.
[100]Wierzbicki A S, Hardman T, Prince W T. Future challenges for microsomal transport protein inhibitors [J]. Current Vascular Pharmacology,2009,7(3):277-286.
[101]Meuwese M C, de de Groot E, Duivenvoorden R, et al. ACAT inhibition and progression of carotid atherosclerosis in patients with familial hypercholesterolemia:the CAPTIVATE randomized trial[J]. J Am Med Assoc,2009,301(11):1131-1139.
[102]Buchwald H, Varco R L, Matts J P, et al. Effect of partial ileal bypass surgery on mortality and morbidity from coronary heart disease in patients with hypercholesterolemia. Report of the program on the surgical control of the hyperlipidemias [J]. N Engl J Med,1990,323(14):946-955.
[103]Yokoyama M, Origasa H, Matsuzaki M, et al. Effects of eicosapentaenoic acid on major coronary events in hypercholesterolaemic patients (JELIS):a randomized open-label, blinded endpoint analysis [J]. Lancet, 2007,369(9567):1090-1098.
[104]Barter P J, Caulfield M, Eriksson M, et al. Effects of torcetrapib in patients at high risk for coronary events [J]. N Engl J Med,2007,357 (21):2109-2122.
[105]Simic B, Hermann M, Shaw S Q et al. Torcetrapib impairs endothelial function in hypertension [J]. Eur Heart J,2012,33(13):1615-1624.
[106]徐乃翠,徐晓春,俞琦,等.他汀类药物治疗高脂血症不良反应的观察与护理干预[J].实用医学杂志,2010,26(10)：1834-1836.
[107]Monika L. Depressive symptoms in hypercholesterolemic patients treated with parvastatin[J]. Lancet, 1992,340 (8824):910.
[108]Cuchel Marina, Bloedon LeAnne T, Szapary Philippe,et al. Inhibition of Microsomal Triglyceride Transfer Protein in Familial Hypercholesterolemia[J]. The New England Journal of Medicine,2007,356 (2): 148-156.
[109]Moghadasiam MH, Mancini GB, FrohlichJJ. pharmacotherapy of hypercholesterolemia:Statins in clinical practice[J]. Expertopin pharmacotherapy,2000,1(4):683-695.
[110]刘桂荣,袁汝明.对高脂血症几个问题的探讨[J].山东中医药大学学报,2001,25(5)：33.
[111]叶世龙,刘爱芹.健脾通脉汤治疗高脂血症临床观察[J].中华中医药杂志,2008,23(10)：916-917.
[112]赵林,赵军绩.渗葛降脂宁治疗冠心痛高脂血症疗效观察[J].湖北中医杂志,1999,21(9)：39.
[113]郭姣,朴胜华.从高脂血症发病低龄化趋势探讨其中医发病机制[J].中医药信息,2008,25(6)：4-5.
[114]中国成人血脂异常防治指南制定联合委员会.中国血脂异常防治指南[J].中华心血管杂志,2007,35(5)：390-419.
[115]薛慧,李玉山,谭志鑫.银杏叶茶对高胆固醉饮食小鼠血脂的影响[J].中国现代医学杂志,2001,11(4)：53.
[116]王德山,肖玉芳,许亚杰.枸杞子对老年性高脂血症降脂作用的临床研究[J].辽宁中医杂志,1996,23(10)：475-476.
[117]陶波,帅景贤,吴凤莲.荷叶水煎剂对高脂血症大鼠血脂及血液流变学的影响[J].中医药学报,2000,7(6)：55-56.
[118]张椒英,张旭辉,杏仁油治疗高脂血症疗效观察[J].中医药研究,2002,18(3)：3.
[119]工洪秀.水蛙胶囊治疗高脂血症56例[J].国医论坛,2002,17(5)：62.
[120]周建英,申冬珠.大黄醇提片降脂与抗动脉粥样硬化的研究[J].山东中医药大学学报,1997,21(1)：46-48.
[121]刘智.黄芩茎叶总黄酮治疗2型糖尿病性高脂血症大鼠的实验研究[J].中药新药与临床药理,2009,20(1)：5-6.
[122]滕宇,张秋菊,齐治家.中医药抗脂肪肝的研究进展[J].北京中医药大学学报(中医临床版),2005,12(2)：37-41.
[123]管淑玉,苏薇薇.何首乌的化学成分和药理作用研究进展[J].中南药学,2008,6(4)：454-455.
[124]贺成宏.通络降脂饮治疗高脂血症50例[J].内蒙古中医药,2008(4)：17.
[125]黄敬文,段剑飞,秦书芝.中药治疗高脂血症作用机理研究进展[J].中国现代实用医学杂志,2006,5(8)：30-32.
[126]王帅.从肝论治高脂血症探要[J].实用中医内科杂志,2008,22(9)：40.
[127]赵宝安.理肝清脂饮治疗高脂血症61例[J].湖南中医杂志,2005,21(3)：69-70.
[128]陈辉先.泻肝活血汤治疗高脂血症33例临床观察[J].湖南中医杂志,2008,24(5)：9-11.
[129]吴娅妮.益肝调脂饮治疗高脂血症37例分析[J].中华现代内科学杂志,2007,4(1)：24-25.
[130]陈佑林,常建国.加味胃苓汤治疗脾虚痰湿中阻型高脂血症56例[J].四川中医,2008,26(11)：85.
[131]安凤华,邹德运.健脾化痰通络法治疗高脂血症体会[J].中华临床医学研究杂志,2007,13(4)：530-531.
[132]胡郁坤,李昆三.保和丸加减治疗高脂血症39例临床观察[J].中国中医药杂志,2008,6(5)：18-20.
[133]肖艳皎,刘延祥.试析高脂血症从脾论治[J].医药卫生,2007,36(4)：194.
[134]冯锦.健脾化痰祛湿方治疗高脂血症脾虚痰浊型56例[J].中国中医药科技,2012,19(1)：93.
[135]吴同启.从脾肝论治高脂血症60例[J].陕西中医,2004,25(2)：133-134.
[136]胡元吉,陈庆.疏肝健脾法治疗高脂血症42例[J].中国实验方剂学杂志,2012,18(13)：291-292.
[137]彭小明.丹参首乌山楂饮对血脂代谢紊乱的影响[J].浙江中医杂志,2006：41(7)：413.
[138]刘立.降脂茶治疗高脂血症260例[J].中国中医药信息杂志,2006,13(8)：48-49.
[139]李恩庆,佟晓辉.补肾降脂方治疗高脂血症55例[J].中国中医基础医学杂志,2006,12(3)：212-213.
[140]李进龙,田元祥.杨牧祥治疗高脂血症经验[J].辽宁中医杂志,2008,35(7)：983.
[141]江伟,张惠勤,王秋萍.活血降脂汤对血瘀型高脂血症降脂作用的临床观察与实验研究[J].中国中医基础医学杂志,2008,14(5)：374.
[142]赵秀玲.调脂汤治疗高脂血症的疗效观察[J].四川中医,2006,24(4)：52-53.
[143]刘兰印,信建军.化瘀祛痰饮治疗高脂血症70例临床观察[J].四川中医,2005,23(2)：56.
[144]阿衣努尔·木合买提巴克,陈健.火树华教授治疗高脂血症的中医临床经验[J].新疆中医药,2007,25(4)：89-90.
[145]曾宪国.加味血府逐瘀汤合辛伐他汀治疗高脂血症36例临床观察[J].中医药导报,2011,17(3)：40.
[146]吴中朝,王玲玲,徐兰凤,等.艾灸对高脂血症调脂作用的研究[J].上海针灸杂志,1997,16(6)：5-6.
[147]吴中朝,王玲玲,刘跃光,等.艾灸对老年人血液载脂蛋白研究[J].中国针灸,1998,(5)：261-262.
[148]吴中朝,王玲玲,刘跃光,等.艾灸降血脂作用研究[J].南京中医药大学学报,1996,12(5)：41-42.
[149]常小荣,严洁,易受乡,等.隔药饼灸治疗血脂异常的临床研究[J].中华中医药学刊,2010,28(1)：8-10.
[150]钱小路,鲍春龄,侯文光,等.隔药饼灸治疗更年期综合征合并高血脂疗效观察[J].河北中医,2010,32(10)：79-81.
[151]高耀华,王竹行,陈新黔等.降脂药灸治疗中老年高脂血症的临床研究[J].中国针灸,2000,(2)：77-78.
[152]邓柏颖,谢感共,罗本华等.功能保健灸治疗高脂血症40例疗效观察[J].新中医,2002,34(9)：48-49.
[153]王国明,沈玲哲,温峰云,等.瘢痕灸治疗高脂血症40例临床观察[J].中国中医药信息杂志,2000,
7(11)：72-73.
[154]李建萍,姚永年,何培达等.艾灸治疗血脂异常患者的临床研究[J].中国针灸,2005,25(11)：825-827.
[155]吴中朝,刘跃光,王玲玲,等.艾灸抗高甘油三酯血症脂质过氧化正交试验临床研究[J].中国针灸,1998(6)：325-327.
[156]牛晓红,金红,宋剑南等.灸神阙降脂抗氧化作用的研究[J].中国中医基础医学杂志,2003,9(10)：71-77.
[157]岳增辉,严洁,常小荣,等.隔药饼灸对高脂血症兔主动脉内皮细胞超微结构的影响[J].中国针灸,2005,25(1)：64-67.
[158]常小荣,严洁,岳增辉,等.隔药饼灸对高脂血症兔血浆ET、NO含量的影响[J].中国中医药信息杂志,2005,12(6)：20-21.
[159]沈菁,常小荣,严洁,等.隔药饼灸对高脂血症兔血浆内皮素及一氧化氮含量的调节[J].中国临床康复,2006,10(27)：184-186
[160]岳增辉,常小荣,严洁,等.隔药饼灸对兔高脂血症合并动脉粥样硬化主动脉血管细胞黏附分子-1mRNA表达的影响[J].针刺研究,2006,31(3)：145-148.
[161]岳增辉,严洁,常小荣,等.隔药饼灸对兔高脂血症合并动脉粥样硬化血管内皮细胞黏附因子E选择素mRNA表达的影响[J].中国针灸,2006,13(7)：37-39.
[162]常小荣,严洁,岳增辉,等.隔药饼灸对高脂血症兔血浆前列环素和血栓素含量的影响[J].中国临 床康复,2008,8(33)：7446-7447.
[163]吴中朝,刘跃光,王玲玲,等HTG艾灸降脂正交设计研究[J].南京中医药大学学报,1998,14(5)：291.
[164]李爱军.隔药饼灸治疗高脂血症的临床研究[J].广西中医药,2007,30(3)：12-13.
[165]Caterina M J, Schumacher MA, Tominaga M, et al. The capsaicin receptor:a heat-activated ion channel in the pain pathway. Nature,1997,389:816-824.
[166]Venkataehalam K, Monteil C. TRP Channels[J].Annu Rev Biochem,2007,76:387-417.
[167]Luo Z, Ma L, Zhao Z, et al. TRPV1 activation improves exercise endurance and energy metabolism through PGC-1 alpha upregulation in mice[J]. Cell Research,2012,22(3):551-564.
[168]Tousova K, Susankova K, Teisinger J, et al. Oxidizing reagent copper-o-phenanthroline is an open channel blocker of the vanilloid receptor TRPVl[J]. Neuropharmacology,2004,47:273-285.
[169]Clapham DE. Snapshot:mammalian TRP channels[J]. Cell,2007,129:220.
[170]Firth AL, Remillard CV, Yuan JX. TRP channels in hypertension[J]. Biochim Biophys Acta,2007,1772: 895-906.
[171]Tousova K, Susankova K, Teisinger J, et al. Oxidizing reagent copperophenanthroline is an open channel blocker of the vanilloid receptor TRPV1[J]. Neuropharmacology,2004,47:273-285.
[172]Ramsey IS, Delling M, Clapham DE. An introduction to TRP channels[J]. Annu Rev Physiol,2006,68: 619-47.
[173]Mandadi S, Tominaga T, Numazaki M, et al. Increased sensitivity of desensitized TRP V1 by PMA occurs through PKCepsilon-mediated phosphory lationatS800[J].Pain,2006,123(1-2):106-16.
[174]ALAWI K, KEEBLE J. The paradoxical role of the transient receptor potential vanilloid 1 receptor in inflammation[J]. Pharmacol Ther,2010,125(2):181-195.
[175]Pandolfi A, Grilli A, Cilli C, et al. Phenotype modulation in cultures of vascular smooth muscle cells from diabetic rats:association with increased nitric oxide synthase expression and superoxide anion generation[J]. J Cell Physiol,2003,196:378-385.
[176]Gunthorpe MJ, Szallasi A. Peripheral TRPV1 receptors as targets for drug development:new molecules and mechanisms[J]. Curr Pharm Des,2008,14:32-41.
[177]Yang XR, Lin MJ, McIntosh LS, et al. Functional expression of transient receptor potential melastatin-and vanilloid-related channels in pulmonary arterial and aortic smooth muscle[J]. Am J Physiol Lung Cell Mol Physiol,2006,290:L1267-1276.
[178]Ma L, Zhong J, Zhao Z, et al. Activation of TRPV1 reduces vascular lipid accumulation and attenuates atherosclerosis[J]. Cardiovasc Res,2011,92(3):504-513.
[179]Bratz I N, Dick G M, Tune J D, et al. Impaired capsaicin-induced relaxation of coronary arteries in a porcine model of the metabolic syndrome[J]. Am J Physiol Heart Circ Physiol,2008,294(6):H2489-2496.
[180]Zhang L L, Yan Liu D, Ma L Q, et al. Activation of transient receptor potential vanilloid type-1 channel prevents adipogenesis and obesity [J]. Circ Res,2007,100(7):1063-1070.
[181]Hwang SW, Cho H, Kwak J, et al. Direct activation of capsaicin receptors by products of lipoxygenases: endogenous capsaicin-like substances. Proc Natl Acad Sci U S A 2000,97:6155-6160.
[182]Zygmunt PM, Petersson J, Andersson DA, Chuang H, Sorgard M, Di Marzo V, et al.Vanilloid receptors on sensory nerves mediate the vasodilator action of anandamide. Nature,1999,400:452-457.
[183]Yoshida T, Inoue R, Morii T, Takahashi N, Yamamoto S, Hara Y, et al. Nitric oxide activates TRP channels by cysteine S-nitrosylation[J]. Nat Chem Biol,2006,2:596-607.
[184]Cheng W, rang F, Takanishi CL, et al. Thermosensitive TRPV channel subunits coassemble into heteromeric channels with intermediate conductance and gating properties[J]. J Gen Physiol,2007,129(3): 191-207.
[185]Baylie R L, Brayden J E. TRPV channels and vascular function[J]. ActaPhysiologica,2011,203 (1):99-116.
[186]Yang D, Luo Z, Ma S, et al. Activation of TRPV1 by Dietary Capsaicin Improves Endothelium Dependent Vasorelaxation and Prevents Hypertension[J]. Cell Metab,2010,12(2):130-141
[187]Poblete I M, Orliac M L, Briones R, et al. Anandamide elicits an acute release of nitric oxide through endothelial TRPV1 receptor activation in the rat arterial mesenteric bed[J]. The Journal of physiology,2005, 568(2):539-551.
[188]Huang W, Wang H, Galligan JJ, et al. Transient recept or pot entail vanilloid subtype 1 channel mediated neuropeptide secretion and depressor effects:role of endoplasmic reticulum associated Ca2+ release receptors in rat dorsal root ganglion neurons[J]. J Hypertens,2008,26(10):1966-1975.
[189]Ahuja, K. D.; Ball, M. J. Effects of daily ingestion of chilli on serum lipoprotein oxidation in adult men and women[J]. The British journal of nutrition,2006,96(2):239-242.
[190]Ahuja K D, Kunde D A, Ball M J, et al. Effects of capsaicin, dihydrocapsaicin, and curcumin on copper-induced oxidation of human serum lipids[J]. J Agric Food Chem,2006,54(17):6436-6439.
[191]Rosa A, Appendino G, Melis M P, et al. Protective effect and relation structure-activity of nonivamide and iododerivatives in several models of lipid oxidation[J]. Chemico-Biological Interactions,2009,180(2): 183-192.
[192]Ohnuki K, Haramizu S, Oki K, et al. Administration of capsiate, a non-pungent capsaicin analog, promotes energy metabolism and suppresses body fat accumulation in mice[J]. Bioscience, biotechnology, and biochemistry,2001,65(12):2735-2740.
[193]Yoshioka M, St-Pierre S, Suzuki M, et al. Effects of red pepper added to high-fat and high-carbohydrate meals on energy metabolism and substrate utilization in Japanese women[J]. The British journal of nutrition, 1998,80(6):503-510.
[194]Zhang LL, Liu DY, Ma LQ, et al. Activation of transient receptor potential vanilloid type-1 channel prevents adipogenesis and obesity [J].Circ Res,2007,100(7):1063-1070.
[195]Manjunatha H, Srinivasan K. Hypolipidemic and ant ioxidant effects of curcumin and capsaicin in high-fat-fed rats[J]. Can J Physiol Pharmacol,2007,85(6):588-596.
[196]GUNTHORPE MJ, SZALLASI A. Peripheral TRPV1 receptors as targets for drug development:new molecules and mechanisms[J]. Curr Pharm Des,2008,14(1):32-41.
[197]Puntambekar P, Van Buren J, Raisinghani M, et al. Direct interaction of adenosine with the TRPV1 channel protein[J]. J Neurosci,2004,24:3663-3667.
[198]杨莉,李亮,朱兵,等.灸法疗效主要影响因素的分析研究[J].世界中医药,2009,4(4)：217-219.
[199]王玲玲.艾灸的特点及温通效应[J].中国针灸,2011,31(10)：865-868.
[200]中国成人血脂异常防治指南制订委员会.中国成人血脂异常防治指南[J].中华心血管杂志,2007,35(5)：390-419.
[201]Cesare P, Moriondo A, VellaniV, et al. Ion channels gated by heat[J]. Proc Natl Acad Sci,1999,96: 765-766.
[202]刘凯,李传富,申冬珠.大鼠高胆固醇血症快速造型法初筛降脂中草药[J].徐州医学院学报,1990,10(4)：260-262.
[203]王乐,王兰兰,曹宇.TRPV1对LPS致热大鼠体温及下丘脑中Ca2+浓度和cAMP含量的影响[J].中国药理学通报,2009,25(1)：51-55.