大鼠肾炎湿热证血尿模型的实验研究
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摘要
目的:
通过建立不同造模方法的血尿模型,比较其相关指标,希望找到更符合中医湿热证,“病证结合”且价格低廉的肾炎血尿动物模型。
方法:
选择50只SPF级雄性Wistar大鼠为实验动物,在口服并定时尾静脉注射牛血清白蛋白(BSA)的基础上给予不同的干预,建立具有系膜增生性改变的湿热证大鼠血尿模型。随机分为5组:①正常组;②模一组,注射葡萄球菌肠毒素B(SEB),不加环境和饮食因素的对照模型组;③模二组,注射SEB,施加环境和饮食湿热因素的改良模型组;④模三组,不注射SEB,施加环境和饮食湿热因素组;⑤模四组,不注射SEB,施加两次环境和饮食湿热因素组。观察动物至十二周末,处死动物。利用生物学方法、放射免疫法、光学显微镜等手段观察各组大鼠一般情况和体温、体重变化,尿红细胞,24小时尿蛋白定量,肾组织病理变化,同时检测各组大鼠的肾功能,血脂四项以及血清中IL-6的含量。
结果:
1.一般情况
各模型组大鼠均出现程度不等的发热、嗜卧、行动呆滞、耸毛、饮水少、食欲不振、肛门红肿充血、大便烂、尿少色深,舌质暗红,有的舌苔稍白腻,模二和模四组部分出现眼眵、腹泻、皮下水肿等表现,且皮下水肿、尿少色深等情况一直持续到实验结束。模三、四组体重较其他组显著增加,至实验结束。增加湿热因素的模型组体温净增值均较对照模型组(模一组)高,差异有统计学意义(P＜0.05)。
2.尿红细胞及尿蛋白测定
2.1尿红细胞:第5周末至12周末,各模型组大鼠尿红细胞数明显增多,并持续至实验结束,与正常组比较有统计学意义(P＜0.01);12周末,模二组尿红细胞数最多,与其他模型组差异有统计学意义;模三、模四组红细胞数少于模一组,差异有统计学意义(P＜0.01,P＜0.05);模四组尿红细胞数较模三组多,差异无统计学意义(P＞0.05)。
2.2尿蛋白:12周末,各模型组尿蛋白较正常组明显增高,差异有统计学意义(P＜0.01);模二组尿蛋白最多,但较模一组差异无统计学意义(P＞0.05);模三组、模四组较模一组少,差异有统计学意义(P＜0.01);模四组尿蛋白量较模三组多,但差异无统计学意义(P＞0.05)。
3.肾功能测定
3.1血尿素氮水平(BUN):各模型组BUN水平较正常组均有所增高,差异有统计学意义(P＜0.05,P＜0.01);模一组BUN水平最高,但与模二、模三,模四组比较差异无统计学意义(P＞0.05);模四组BUN水平较模三组高,但差异无统计学意义(P＞0.05)。
3.2血肌酐水平(Scr):各模型组Scr水平较正常组明显增高,差异有统计学意义(P＜0.01);模二组Scr水平最高,与模一组比较差异有统计学意义(P＜0.01),模三、模四组Scr水平较模一组高,差异无统计学意义(P＞0.05);模四组Scr水平较模三组高,但差异无统计学意义(P＞0.05)。
4.血脂水平测定
4.1血清总胆固醇(CHOL):各模型组CHOL水平较正常组明显增高,差异有统计学意义(P＜0.01);模二组CHOL水平最高,与模一组比较差异有统计学意义(P＜0.05),模三CHOL水平较模一组低、模四组CHOL水平较模一组高,但差异无统计学意义(P＞0.05);模四组的CHOL水平较模三组高,但差异无统计学意义(P＞0.05)。
4.2血清甘油三酯(TG):各模型组TG水平较正常组明显增高,差异有统计学意义(P＜0.05,P＜0.01);模二组TG水平最高,与模一组比较差异有统计学意义(P＜0.05),模三组TG水平较模一组低,差异无统计学意义(P＞0.05),模四组TG水平较模一组高,差异有统计学意义(P＜0.05);模四组TG水平较模三组高,差异有统计学意义(P＜0.05)。
4.3血清高密度脂蛋白胆固醇(HDL-C)、血清低密度脂蛋白胆固醇(LDL-C):各组实验大鼠血清HDL-C和LDL-C水平之间均无统计学意义(P＞0.05)。
5.血清白细胞介素6(IL-6)水平测定:各模型血清IL-6水平较正常组明显增高,差异有统计学意义(P＜0.01);模二组血清IL-6水平最高,与模一组比较差异有有统计学意义(P＜0.05);模三、模四组血清IL-6水平低于模一组,差异有统计学意义(P＜0.01);模四组血清IL-6水平高于模三组,但无统计学意义(P＞0.05)。
6.病理组织学观察
6.1光镜组织学变化:光镜下,正常组大鼠肾小球系膜细胞及基质无增生,毛细血管襻开放,肾小管结构规则,间质无增生及炎细胞浸润。各模型组大鼠可见弥漫性肾小球系膜区增宽,系膜细胞、系膜基质增生,毛细血管腔狭窄,部分肾小球萎缩,个别肾小球呈分叶状,肾小囊轻度扩张,肾小管间质有炎细胞浸润。尤其是模二组病理改变最为显著,模型一组与二组差异不明显;模三、模四组病理改变与模一、二组相似,但没有上述两组显著,模三与模四组比较无明显差异。
结论:
我们根据中医有关湿热证的病因病理学理论,利用综合因素,成功制成了具有湿热证改变的大鼠系膜增生性肾炎血尿模型。与传统造摸方法比较,施加饮食、环境湿热因素后,能升高大鼠的体温,加重大鼠血尿、水肿及血清总胆固醇、甘油三酯、IL-6、血肌酐水平,使其湿热表现更为突出。该模型无论从证的表现到病的特征,从发病条件到微观指标,都与人类肾炎湿热证型近似,是“病证结合”较好的肾炎湿热证血尿动物模型。而不注射SEB,仅增加饮食、环境湿热因素所制成的肾炎血尿模型,是病理改变典型且价格低廉的肾炎湿热证血尿动物模型。
Objectives:
To explore an animal model of nephritis hematuria that more compatible to the Damp-Heat syndrome and less expensive in cost and more sticking to the "Syndrome closely related to disease" via comparing indexes in different modeled rats.
Methods:
50 SPF male Wistar rats were used to establish models of nephritis hematuria with damp-heat syndrome, rats were give different treatment based on intragastric administration and regular tail vein injection of bovine serum albumin (BSA), they ware randomly divided into five groups as follows:①normal group;②model group one, injected staphylococcal enterotoxin B (SEB) and fed with high-carbohydrate diet, high fat diet, under an environment of high temperature and high humidity;③model group two, an improved model group which was injected SEB and given damp-heat factors of environment and diet;④model group three, given damp-heat factors of environment and diet and no SEB;⑤model group four: injected SEB and given twice damp-heat factors of environment and diet. Animals were raised under observation and killed at the end of 12 weeks. For each group, general condition, body temperature and the body weight, urine red blood cells, 24-hour urine protein, kidney pathological changes of rats were observed, along with the renal function, 4 items of blood lipids (total serum cholesterol, serum triglycerides, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol), and serum IL-6 content in rats were detected by biological methods, RIA, optical microscopes.
Results:
1. General status:
It appears that rats in each groups manifested fever temperature, preferring lying, sluggish action, erecting hair, drinking less, loss of appetite, congestive inflamed anus, rarefaction stool, urine dark in color and less in volume, dark red tongue, some slightly white and greasy fur. Some of the rats in the group two and four have gum in the eyes, diarrhea, skin edema performance, and the phenomenon of subcutaneous edema, urine in dark color and less volume continued to the end of the experiment. Body weight of rats in group three and four were increased significantly than the other groups to the end of the experiment. The rats net value-added of body temperature in model group that given damp-heat factor was higher than that in other control model group (group one) and the differences were significant (P <0.05).
2. Detection of urine red blood cell and urine protein:
2.1 Urine red blood cells: From the end of the 5th and the end of 12th weeks, as compared with normal group, the number of urine red blood cells increased significantly in each model groups, the differences were significant (P <0.01), and continued to the end of the experiment. At the end of the 12th week, as compared with the other groups, the group two had the largest number of urine red blood cells, and had a significant difference from other model groups. Urine red blood cells of group three and four were less than group one, and also had a significant difference (P <0.01, P <0.05), moreover, the group four had more than the group three, The difference was not significant (P> 0.05).
2.2 Urine protein: At the end of the 12th week, as compared with the other model groups, the model group urine protein was significantly higher than normal group, it had a significant difference (P<0.01). Group two had the largest number of urine protein among all group. The difference between group and group one was not significant (P>0.05). The differences between group one and group three and four were significant (P>0.05), but the difference between model group four and group three was not significant (P>0.05) though model group four demonstrated seemingly higher.
3. Determination of renal function
3.1 Blood urea nitrogen level (BUN): The level of BUN in model groups were higher than the normal group, the differences were significant (P< 0.05, P<0.01). The level of BUN in group one was highest, but as compared to other groups, it had no significance (P>0.05). The level of group four was higher than group three, but with no significance (P>0.05).
3.2 Level of blood Scr: The model groups were higher than the normal group obviously, and the differences were significant (P<0.01). The level of group two was highest, and as compared to group one, the difference was significant (P<0.01), the level of group three and four were higher than group one, but the difference was not significant(P>0.05).The level of group four was higher than group three, but the difference wasn't significant(P>0.05).
4. Determination of blood-lipid level
4.1 Serum total cholesterol (CHOL): the level of CHOL model groups was higher than normal groups, the differences was significant (P<0.01). The level of group two was highest, and the difference was significant compared to group one (P< 0.01), the level of group three and four were higher than group one, but the difference was not significant (P>0.05). The level of group four was higher than group three, but the difference was not significant (P>0.05).
4.2 Serum total triglyceride(TG): the level of TG model groups was higher than normal groups, the differences was significant(P<0.01).The level of group two was highest, and the difference was significant as compared to group one(P<0.01),the level of group three and four were higher than group one, but the difference wasn't significant(P>0.05). The level of group four was higher than group three, but the difference wasn't significant (P>0.05).
4.3 Serum total high-density lipoprotein (HDL-C), serum total low-density lipoprotein (HDL-C): the difference of the level in HDL-C and HDL-C among all the groups weren't significant (P>0.05).
5 The level of IL-6:
The level of IL-6 in all model groups was higher than normal groups, and the difference was significant (P< 0.01) ; The level of group two was highest, and the difference was significant compared to group one(P< 0.01),the level of group three and four were higher than group one, but the difference wasn't significant(P>0.05).The level of group four was higher than group three, but the difference wasn't significant(P>0.05).
6. Observation on Histopathology:
Histological changes were observed under light microscope, we can see the mesangial cells and glomerular basement membrane were not proliferate, the capillary loop open. the structure of glomerular atrophy tubular is normal, and stromal hyperplasia and infiltration of inflammatory cells were not observed in the normal group. In the other model groups, diffuse mesangial area was seen widened. The mesangial cells and glomerular basement membrane were proliferating, cavity of capillaries became narrow , Some of the glomerulars atrophied, some was phyllodes, renal capsule mildly expanded, tubulointerstitial have infiltration of inflammatory cells, especially the pathological changes of group two were the most severe, no significant difference was seen between model group one and model group two. The model group three and model group four showed similar changes to that of model group one and two, but with less significance. No obvious difference was observed in comparison between model group three and four.
Conclusions:
According to the damp-heat pathogen of the Chinese medicine theory, using the composite factor, we successfully established rat models of nephritis hematuria with damp-heat syndrome. When compared with traditional method, exerting the factor of diet and damp-heat environment can raise the temperature of rat, make a more severe hematuria edema, higher contents of Scr, triglyceride, cholesterol, IL-6, creatinine, and made the damp-heat symptom more prominently. Whether from the manifestation of symptom to the characteristic of disease or from the onset condition to microcosmic norm, this model, which is similar to human damp-heat nephritis, is a better animal hematuria one for damp-heat nephritis with the "syndrome closely related to disease". Animal model with damp-heat syndrome of nephritis hematuria, which was given no SEB injection and only more food and damp-heat factor, was an animal model whose method was cheaper and more typically than others.
通过建立不同造模方法的血尿模型,比较其相关指标,希望找到更符合中医湿热证,“病证结合”且价格低廉的肾炎血尿动物模型。
方法:
选择50只SPF级雄性Wistar大鼠为实验动物,在口服并定时尾静脉注射牛血清白蛋白(BSA)的基础上给予不同的干预,建立具有系膜增生性改变的湿热证大鼠血尿模型。随机分为5组:①正常组;②模一组,注射葡萄球菌肠毒素B(SEB),不加环境和饮食因素的对照模型组;③模二组,注射SEB,施加环境和饮食湿热因素的改良模型组;④模三组,不注射SEB,施加环境和饮食湿热因素组;⑤模四组,不注射SEB,施加两次环境和饮食湿热因素组。观察动物至十二周末,处死动物。利用生物学方法、放射免疫法、光学显微镜等手段观察各组大鼠一般情况和体温、体重变化,尿红细胞,24小时尿蛋白定量,肾组织病理变化,同时检测各组大鼠的肾功能,血脂四项以及血清中IL-6的含量。
结果:
1.一般情况
各模型组大鼠均出现程度不等的发热、嗜卧、行动呆滞、耸毛、饮水少、食欲不振、肛门红肿充血、大便烂、尿少色深,舌质暗红,有的舌苔稍白腻,模二和模四组部分出现眼眵、腹泻、皮下水肿等表现,且皮下水肿、尿少色深等情况一直持续到实验结束。模三、四组体重较其他组显著增加,至实验结束。增加湿热因素的模型组体温净增值均较对照模型组(模一组)高,差异有统计学意义(P＜0.05)。
2.尿红细胞及尿蛋白测定
2.1尿红细胞:第5周末至12周末,各模型组大鼠尿红细胞数明显增多,并持续至实验结束,与正常组比较有统计学意义(P＜0.01);12周末,模二组尿红细胞数最多,与其他模型组差异有统计学意义;模三、模四组红细胞数少于模一组,差异有统计学意义(P＜0.01,P＜0.05);模四组尿红细胞数较模三组多,差异无统计学意义(P＞0.05)。
2.2尿蛋白:12周末,各模型组尿蛋白较正常组明显增高,差异有统计学意义(P＜0.01);模二组尿蛋白最多,但较模一组差异无统计学意义(P＞0.05);模三组、模四组较模一组少,差异有统计学意义(P＜0.01);模四组尿蛋白量较模三组多,但差异无统计学意义(P＞0.05)。
3.肾功能测定
3.1血尿素氮水平(BUN):各模型组BUN水平较正常组均有所增高,差异有统计学意义(P＜0.05,P＜0.01);模一组BUN水平最高,但与模二、模三,模四组比较差异无统计学意义(P＞0.05);模四组BUN水平较模三组高,但差异无统计学意义(P＞0.05)。
3.2血肌酐水平(Scr):各模型组Scr水平较正常组明显增高,差异有统计学意义(P＜0.01);模二组Scr水平最高,与模一组比较差异有统计学意义(P＜0.01),模三、模四组Scr水平较模一组高,差异无统计学意义(P＞0.05);模四组Scr水平较模三组高,但差异无统计学意义(P＞0.05)。
4.血脂水平测定
4.1血清总胆固醇(CHOL):各模型组CHOL水平较正常组明显增高,差异有统计学意义(P＜0.01);模二组CHOL水平最高,与模一组比较差异有统计学意义(P＜0.05),模三CHOL水平较模一组低、模四组CHOL水平较模一组高,但差异无统计学意义(P＞0.05);模四组的CHOL水平较模三组高,但差异无统计学意义(P＞0.05)。
4.2血清甘油三酯(TG):各模型组TG水平较正常组明显增高,差异有统计学意义(P＜0.05,P＜0.01);模二组TG水平最高,与模一组比较差异有统计学意义(P＜0.05),模三组TG水平较模一组低,差异无统计学意义(P＞0.05),模四组TG水平较模一组高,差异有统计学意义(P＜0.05);模四组TG水平较模三组高,差异有统计学意义(P＜0.05)。
4.3血清高密度脂蛋白胆固醇(HDL-C)、血清低密度脂蛋白胆固醇(LDL-C):各组实验大鼠血清HDL-C和LDL-C水平之间均无统计学意义(P＞0.05)。
5.血清白细胞介素6(IL-6)水平测定:各模型血清IL-6水平较正常组明显增高,差异有统计学意义(P＜0.01);模二组血清IL-6水平最高,与模一组比较差异有有统计学意义(P＜0.05);模三、模四组血清IL-6水平低于模一组,差异有统计学意义(P＜0.01);模四组血清IL-6水平高于模三组,但无统计学意义(P＞0.05)。
6.病理组织学观察
6.1光镜组织学变化:光镜下,正常组大鼠肾小球系膜细胞及基质无增生,毛细血管襻开放,肾小管结构规则,间质无增生及炎细胞浸润。各模型组大鼠可见弥漫性肾小球系膜区增宽,系膜细胞、系膜基质增生,毛细血管腔狭窄,部分肾小球萎缩,个别肾小球呈分叶状,肾小囊轻度扩张,肾小管间质有炎细胞浸润。尤其是模二组病理改变最为显著,模型一组与二组差异不明显;模三、模四组病理改变与模一、二组相似,但没有上述两组显著,模三与模四组比较无明显差异。
结论:
我们根据中医有关湿热证的病因病理学理论,利用综合因素,成功制成了具有湿热证改变的大鼠系膜增生性肾炎血尿模型。与传统造摸方法比较,施加饮食、环境湿热因素后,能升高大鼠的体温,加重大鼠血尿、水肿及血清总胆固醇、甘油三酯、IL-6、血肌酐水平,使其湿热表现更为突出。该模型无论从证的表现到病的特征,从发病条件到微观指标,都与人类肾炎湿热证型近似,是“病证结合”较好的肾炎湿热证血尿动物模型。而不注射SEB,仅增加饮食、环境湿热因素所制成的肾炎血尿模型,是病理改变典型且价格低廉的肾炎湿热证血尿动物模型。
Objectives:
To explore an animal model of nephritis hematuria that more compatible to the Damp-Heat syndrome and less expensive in cost and more sticking to the "Syndrome closely related to disease" via comparing indexes in different modeled rats.
Methods:
50 SPF male Wistar rats were used to establish models of nephritis hematuria with damp-heat syndrome, rats were give different treatment based on intragastric administration and regular tail vein injection of bovine serum albumin (BSA), they ware randomly divided into five groups as follows:①normal group;②model group one, injected staphylococcal enterotoxin B (SEB) and fed with high-carbohydrate diet, high fat diet, under an environment of high temperature and high humidity;③model group two, an improved model group which was injected SEB and given damp-heat factors of environment and diet;④model group three, given damp-heat factors of environment and diet and no SEB;⑤model group four: injected SEB and given twice damp-heat factors of environment and diet. Animals were raised under observation and killed at the end of 12 weeks. For each group, general condition, body temperature and the body weight, urine red blood cells, 24-hour urine protein, kidney pathological changes of rats were observed, along with the renal function, 4 items of blood lipids (total serum cholesterol, serum triglycerides, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol), and serum IL-6 content in rats were detected by biological methods, RIA, optical microscopes.
Results:
1. General status:
It appears that rats in each groups manifested fever temperature, preferring lying, sluggish action, erecting hair, drinking less, loss of appetite, congestive inflamed anus, rarefaction stool, urine dark in color and less in volume, dark red tongue, some slightly white and greasy fur. Some of the rats in the group two and four have gum in the eyes, diarrhea, skin edema performance, and the phenomenon of subcutaneous edema, urine in dark color and less volume continued to the end of the experiment. Body weight of rats in group three and four were increased significantly than the other groups to the end of the experiment. The rats net value-added of body temperature in model group that given damp-heat factor was higher than that in other control model group (group one) and the differences were significant (P <0.05).
2. Detection of urine red blood cell and urine protein:
2.1 Urine red blood cells: From the end of the 5th and the end of 12th weeks, as compared with normal group, the number of urine red blood cells increased significantly in each model groups, the differences were significant (P <0.01), and continued to the end of the experiment. At the end of the 12th week, as compared with the other groups, the group two had the largest number of urine red blood cells, and had a significant difference from other model groups. Urine red blood cells of group three and four were less than group one, and also had a significant difference (P <0.01, P <0.05), moreover, the group four had more than the group three, The difference was not significant (P> 0.05).
2.2 Urine protein: At the end of the 12th week, as compared with the other model groups, the model group urine protein was significantly higher than normal group, it had a significant difference (P<0.01). Group two had the largest number of urine protein among all group. The difference between group and group one was not significant (P>0.05). The differences between group one and group three and four were significant (P>0.05), but the difference between model group four and group three was not significant (P>0.05) though model group four demonstrated seemingly higher.
3. Determination of renal function
3.1 Blood urea nitrogen level (BUN): The level of BUN in model groups were higher than the normal group, the differences were significant (P< 0.05, P<0.01). The level of BUN in group one was highest, but as compared to other groups, it had no significance (P>0.05). The level of group four was higher than group three, but with no significance (P>0.05).
3.2 Level of blood Scr: The model groups were higher than the normal group obviously, and the differences were significant (P<0.01). The level of group two was highest, and as compared to group one, the difference was significant (P<0.01), the level of group three and four were higher than group one, but the difference was not significant(P>0.05).The level of group four was higher than group three, but the difference wasn't significant(P>0.05).
4. Determination of blood-lipid level
4.1 Serum total cholesterol (CHOL): the level of CHOL model groups was higher than normal groups, the differences was significant (P<0.01). The level of group two was highest, and the difference was significant compared to group one (P< 0.01), the level of group three and four were higher than group one, but the difference was not significant (P>0.05). The level of group four was higher than group three, but the difference was not significant (P>0.05).
4.2 Serum total triglyceride(TG): the level of TG model groups was higher than normal groups, the differences was significant(P<0.01).The level of group two was highest, and the difference was significant as compared to group one(P<0.01),the level of group three and four were higher than group one, but the difference wasn't significant(P>0.05). The level of group four was higher than group three, but the difference wasn't significant (P>0.05).
4.3 Serum total high-density lipoprotein (HDL-C), serum total low-density lipoprotein (HDL-C): the difference of the level in HDL-C and HDL-C among all the groups weren't significant (P>0.05).
5 The level of IL-6:
The level of IL-6 in all model groups was higher than normal groups, and the difference was significant (P< 0.01) ; The level of group two was highest, and the difference was significant compared to group one(P< 0.01),the level of group three and four were higher than group one, but the difference wasn't significant(P>0.05).The level of group four was higher than group three, but the difference wasn't significant(P>0.05).
6. Observation on Histopathology:
Histological changes were observed under light microscope, we can see the mesangial cells and glomerular basement membrane were not proliferate, the capillary loop open. the structure of glomerular atrophy tubular is normal, and stromal hyperplasia and infiltration of inflammatory cells were not observed in the normal group. In the other model groups, diffuse mesangial area was seen widened. The mesangial cells and glomerular basement membrane were proliferating, cavity of capillaries became narrow , Some of the glomerulars atrophied, some was phyllodes, renal capsule mildly expanded, tubulointerstitial have infiltration of inflammatory cells, especially the pathological changes of group two were the most severe, no significant difference was seen between model group one and model group two. The model group three and model group four showed similar changes to that of model group one and two, but with less significance. No obvious difference was observed in comparison between model group three and four.
Conclusions:
According to the damp-heat pathogen of the Chinese medicine theory, using the composite factor, we successfully established rat models of nephritis hematuria with damp-heat syndrome. When compared with traditional method, exerting the factor of diet and damp-heat environment can raise the temperature of rat, make a more severe hematuria edema, higher contents of Scr, triglyceride, cholesterol, IL-6, creatinine, and made the damp-heat symptom more prominently. Whether from the manifestation of symptom to the characteristic of disease or from the onset condition to microcosmic norm, this model, which is similar to human damp-heat nephritis, is a better animal hematuria one for damp-heat nephritis with the "syndrome closely related to disease". Animal model with damp-heat syndrome of nephritis hematuria, which was given no SEB injection and only more food and damp-heat factor, was an animal model whose method was cheaper and more typically than others.
引文
1 Levey AS,Eckardt KU,Tsukamoto Y,et al.Definition and classification of chronic kidney disease apposition statement from Kidney Disease:Improving Global Outcomes(KDIGO).Kidney Int,2005,67(6):2089-2100.
2 胡海翔,贾海骅.滋肾止血片对实验性IgA肾病大鼠治疗作用的实验研究. 中国中医基础医学杂志,1999,5(1):39-44.
3 吴仕九,杨运高.温病湿热证动物模型的研制及清祛湿法机理的探讨.中国中医药科技,1999,6:65-67.
4 全国儿科肾脏病学组.儿童泌尿系疾病流行病学调查-全国21省市尿过筛检查小结.中华儿科杂志,1989,27(6):344-346.
5 中华医学会儿科学会肾脏病学组.我国小儿肾小球疾病肾组织病理改变:2315例肾活检材料的综合分析.中华儿科杂志,1996,34(5):319-323.
6 钱铜荪 主编.肾脏病学(第三版).北京:华夏出版社,2001,173.
7 陈惠萍,曾彩虹.10594例肾活检病理资料分析.肾脏病与透析肾移植杂志,2000,9(6):501-509.
8 黄建萍,刘翠华.无症状肾小球性血尿63例临床与病理.实用儿科临床杂志,1999,14(4):192-194.
9 高远赋,刘光陵.小儿孤立性血尿的病理分析.肾脏病与透析肾移植杂志,2000,9(1):52-53.
10许瑞英,王培荣.血尿原因待查患儿的临床与病理分析.中国实用儿科杂志,2000,15(8):483-485.
11 Piqueras hi,White RH,Raafat F,et al.Renal biopsy diagnosis in children presenting with haematuria.Pediatr Nephrol,1998,12(5):386-391.
12 傅海东,刘爱民,王亚萍,等.91例无症状性血尿患儿临床和病理分析.浙江医学,2006,28(4):286-287.
13 张桂菊,沈颖.儿童单纯性血尿105例病理分析.北京医学,2004,26(4):254-256.
14 张镜人.慢性肾功能不全的证治探讨.上海中医药杂志,1982,(2):11-13
15 赵金锋.肾炎治疗宜存精去粗兼顾.肾炎尿毒症专辑.中医古籍出版社,1988.145.
16 刘志明.肾炎尿毒症专辑.中医古籍出版社,1988.66.
17 阮诗玮,郑敏麟,王智等.Igh肾病湿热证与肾穿刺活检病理组织关系的临床研究.中国中西医结合肾病杂志,2003,4(10):583-584.
18 陆鸿滨.原发性肾小球病湿热证100例分析.贵阳中医学院学报,1986,(2):30
19 余江毅,熊宁宁,余承惠,等.肾炎湿热病理的临床分析和实验研究.中国中西医结合杂志,1992,12(8):458-460.
20 徐大基.原发性肾小球疾病病理类型与中医证型分析.福建中医药,1999.30:18-19.
21 刘宏伟.原发性肾小球疾病湿热病理的临床研究.中医杂志,1996,37(11):688
22 王付民.慢性肾小球肾炎病理类型与中医分型相关性研究.辽宁中医杂志,1994,21(9):391-392.
23 陈香美,陈以平,李平,等.1016例IgA肾病患者中医证候的多中心流行病学调查及相关因素分析.中国中西医结合杂志,2006.(26)3:197-201.
24 胡仲仪,陈以平,查平,等.慢性肾小球肾炎病理分型与中医治疗分析.中国中西医结合杂志,1992,12(8):455-457.
25 叶景华.慢性肾炎中医药研究现状及展望.山东中医杂志,1994,13(1):11-13
26 沈庆法.肾脏病湿热证的研究.浙江中医学院学报,2000,24(1):39-42.
27 王海燕主编.肾脏病学(第二版).北京:人民卫生出版社,1996,648.
28 黎磊石,刘志红,陈惠萍,等.从临床角度认识系膜IgA肾病.中华肾脏病杂志,1992,8(2):106-110.
29 孙伟.第十二次全国中医肾病学术会议论文汇编,1997.
30 Tao K,Nicholls K,Rockman S,et al.Expression of complemento3receptors on neutrophils and erythrocytes in patients with IgA nephropathty.Clin Nephrol,1989,32:203:1990,34:103.
31 叶小玲,黄庆元,郑法雷,等.肾小球肾炎转归与细胞凋亡.国外医学,泌尿系统分册,1998,18(1):11.
32 张曦,赵从禄,等.原发性系膜增生性肾炎患者血小板活化状态的研究.中国中西医结合肾病杂志,2002,3(3):169-170.
33 聂莉芳,方芳.益气滋肾冲剂对IgA肾病小鼠蛋白尿及肾功能的影响.上海 中医药杂志,2000,34(3):45-47.
34 徐巍,张玉梅,吴茜,等.肾炎II号治疗IgA肾病血尿的实验研究.中国中医药科技,2002,9(1):26-27.
35 周家俊,高建东,何立群,等.固本通络冲剂治疗IgA肾病的实验研究.中国中西医结合肾病杂志,2003,(48):442-444.
36 余江毅,熊宁宁,余承惠,慢性肾病瘀血与湿热病理的临床和实验研究.辽宁中医杂志,1995,22(2):91-92.
37 刘宏伟.原发性肾小球疾病湿热病理的临床研究.中医杂志,1996,37(11):688-689
38 廖荣鑫,吴仕九,文小敏,等.脾胃湿热证热偏重、湿热并重型大鼠模型血液中胃动素(MTL)、胃泌素(GAS)的变化研究.浙江中医杂志,2005,40(4):171-173.
39 高清华,陈梁,吕文亮,等.清热化湿法对温病湿热证大鼠SP、SS水平影响的研究.湖北中医学院学报,2005,7(4):12-13.
40 廖礼兵,吴仕九,刘德传.清香散对湿热证大鼠中分子与巯基物质的影响.中国中医药科技,2002,9(1):44-44.
41 佟丽,陈江华.多因素所致温病温热证模型大鼠红细胞免疫功能的变化.中国免疫学杂志,1999,15(8):366-368.
42 吕文亮,柯裕枝,高清华,等.清热化湿法对温病湿热证大鼠抗利尿激素的影响.湖北中医学院学报,2005,7(4):7-9.
43 熊宁宁.家兔肾炎湿热证模型的实验研究.辽宁中医杂志,1991,18(4):42-43
44 朱辟疆,施荣华,刘永平.慢性肾小球疾病湿热证血浆及尿白介素-6的改变.浙江中西医结合杂志,1999,9(2):75-77.
45 Taniguchi Y,YoriokaN,Kumagai J,et al.Interleukin-6 localization and the prognosis of Igh nephropathy.Nephron JT-Nephron,1999,81(1):94-98.
1.王海燕主编.肾脏病学(第二版).北京:人民卫生出版社,1996,648。
2.钱铜荪主编.肾脏病学(第三版).北京:华夏出版社,2001,173。
3.Hawn CVZ,Janeway C.Histologic and serological sequences experimental hypersensitivity.J Exp Med,1947,85:571-590.
4.Germuth FG Jr,Taylor JJ,Siddiqui SY,et al.Immune complex disease.Ⅵ.Some determinants of the varieties of glomerular lesions in the chronic bovine serum albumin-rabbit system.Lab Invest,1977,37:162-169.
5.章友康.家兔慢性血清病所致系膜增殖型肾炎的改进探讨.中华肾脏病杂志,1986,2(1):2-4
6.贾慧,邹万忠.改良慢性血清病性大鼠系膜增生性肾炎模型的建立.肾脏病与透析肾移植杂志,1996,5(3):21-25.
7.Bagchus WM,Jeunink MF,Elema JD.The mesangium in anti-Thy-1nephritis.Influx of macrophages,mesangial cell hypercellularity,and macromolecular accumulation.Am J Pathol,1990,137:215-223.
8.Yamamoto T,et al.Anti-Thymocytc antibody induced mesangialytic nephritis.In:Hatano M,ed.Nephrology.Tokyo:Springer-Verlag,1991:1004.
9.刘志红,黎磊石,杨俊伟,等.抗Thy-1抗体与炎症因子诱发的系膜增殖性肾炎模型.中华肾脏病杂志,1993,9(2):95-96.
10.刘震,周树录,谭建三.大鼠系膜增生性肾模型的复制与改进.华西医科大学学报,1996,27(2):182-184.
11.黄怀鹏,陈志强,陈玉林,等.肾疏宁对大鼠系膜增生性肾炎的实验研究.中医药学刊,2003,21(2):271-272.
12.Miyawaki S,Muso E,Takeuchi E,et al.Selective breeding for high serum IgA levels from noninbred ddY mice:isolation of a strain with an early onset of glomerular Igh deposition.Nephron,1997,76:201-207.
13.Imai H,Nakamoto Y,Asakura K,et al.Spontaneous glomerular Igh deposition in ddY mice:an animal model of IgA nephritis.Kidney Int,1985,27:756-761.
14.hmore A,Roccatello D,Picciotto G,et al.Processing of Igh aggregates in a rat model of chronic liver disease.Clin Immunol Immunopathol,1997,84:107-114.
15.Melvin T,Burke B,Michael AF,et al.Experimental IgA nephropathy in bile duct ligated rats.Clin Immunol Immunopathol,1983,27:369-77.
16.Sato M,Ideura T,Koshikawa S.Experimental IgA nephropathy in mice.Lab Invest,1986,54:377-384.
17.Woodroffe AJ,Gormly AA,Clarkson AR,et al.Experimental cirrhosis and deposition of glomerular IgA immune complexes.Contrib Nephrol,1984,40:51-54.
18.邹万忠,韩可汉.补体在IgA肾病发生中的作用.中华肾脏病杂志,1992,8(6):333-336.
19.Rifai A,Small PA Jr,Teague PO,et al.Experimental IgA nephropathy.J Exp Med,1979,150:1161-1173.
20.Isaacs K,Miller F,Lane B.Experimental model for IgA nephropathy.Clin Immunol Immunopathol,1981,20:419-26.
21.Emancipator SN,Gallo GR,Lamm ME.Experimental IgA nephropathy induced by oral immunization.J Exp Med,1983,157:572-582.
22.章友康,王海燕.肝脏与IgA肾病的关系及其机制的探讨.北京医科大学学报,1988,20(4):257-260.
23.王丽,章友康,王海燕,等.肝脾和(或)胃肠粘膜免疫在肾小球系膜区IgA 沉积中的作用.中华内科杂志,1988,27(4):216-220.
24.刘志红,黎磊石,李莉.葡萄球菌肠毒素诱发的IgA肾病模型.中华肾脏病杂志,1989,5(1):6-10.
25.胡海翔,贾海骅.滋肾止血片对实验性IgA肾病大鼠治疗作用的实验研究.中国中医基础医学杂志,1999,5(1):39-44.
26.刘宏伟,卢景芬.滋肾止血片对实验性IgA肾病小鼠肾组织氧自由基的影响.中国中医基础医学杂志,1996,2:24-26.
27.胡顺金,曹恩泽,张敏,等.康肾止血颗粒剂对IgA肾病模型大鼠作用的实验研究.中医药临床杂志,2005,17(6):574-575.
28.刘志红,黎磊石.葡萄球菌肠毒素诱发的IgA肾病模型.中华肾脏病杂志,1989,5(1):6-10.
29.聂莉芳,方芳.益气滋肾冲剂对IgA肾病小鼠蛋白尿及肾功能的影响.上海中医药杂志,2000,34(3):45-47.
30.张远铮,白克敏,王宝琳.关于补体膜攻击复合物C56-9与实验性IgA肾病及人类IgA肾病可能致病作用的探讨.中华医学会第四次全国肾脏病学术会议论文汇编.1994,10
31.熊宁宁.家兔肾炎湿热证模型的实验研究.辽宁中医杂志,1991.18(4).42-43
32.李仕梅 主编.临床肾脏病学.上海:上海科技出版社,1986,254.
1 杨开清,林培政.清热化湿消瘀法对兔主动脉粥样硬化形成干预作用的超微结构研究.广州中医药大学学报,2006,2 3:318-321.
2 王新华.温病湿热证病理造型及实验研究.广州中医学院学报,1990,7:182-186.
3 吴仕九,杨运高.温病湿热证动物模型的研制及清祛湿法机理的探讨.中国中医药科技,1999,6:65-67.
4 郭明阳,阎翔.温病湿热证湿重于热动物模型的研究.成都中医药大学学报,2003,26:33-36.
5 廖荣鑫,吴仕九,文小敏,等.脾胃湿热证热偏重、湿热并重型大鼠模型血液中胃动素(MTL)、胃泌素(GAS)的变化研究.浙江中医杂志,2005,40:171-173.
6 阎翔,郭明阳.温病湿热证湿重于热动物模型舌的病理观察.安徽中医学院学报,2005,24:19-21.
7 高清华,陈梁,吕文亮,等.清热化湿法对温病湿热证大鼠SP、SS水平影响的研究.湖北中医学院学报,2005,7:12-13.
8 佟丽,陈江华.多因素所致温病温热证模型大鼠红细胞免疫功能的变化. 中国免疫学杂志,1999,15:366-368.
9 文彬,贺松其,吴仕九,等.清热祛湿方对肝纤维化大鼠肝组织SOD、MDA及超微结构的影响.上海中医药杂志,2005,39:56-58。
10吴仕九,杨运高,等.中医湿热证证候模型的应用研究.中医杂志,2001,42:553-555.
11 刘德传,吴仕九,等.清香散对湿热证模型大鼠—氧化氮含量的影响.中国中西医结合消化杂志,2001,9:131-132.
12 刘德传,吴仕九,等.微量元素、抗氧化剂与湿热证的相关性的研究.广东微量元素科学,2001,8:30-32.
13 廖礼兵,吴仕九,等.清香散对湿热证大鼠中分子与巯基物质的影响.中国中医药科技,2002,9:44-44.
14 吴仕九,廖礼兵,文小敏,等.温病湿热证湿热量化的相关性实验研究.中医杂志,2003,44:688-690.
15 吕文亮,柯裕枝,高清华,等.清热化湿法对温病湿热证大鼠抗利尿激素的影响.湖北中医学院学报,2005,7:7-9.
2 胡海翔,贾海骅.滋肾止血片对实验性IgA肾病大鼠治疗作用的实验研究. 中国中医基础医学杂志,1999,5(1):39-44.
3 吴仕九,杨运高.温病湿热证动物模型的研制及清祛湿法机理的探讨.中国中医药科技,1999,6:65-67.
4 全国儿科肾脏病学组.儿童泌尿系疾病流行病学调查-全国21省市尿过筛检查小结.中华儿科杂志,1989,27(6):344-346.
5 中华医学会儿科学会肾脏病学组.我国小儿肾小球疾病肾组织病理改变:2315例肾活检材料的综合分析.中华儿科杂志,1996,34(5):319-323.
6 钱铜荪 主编.肾脏病学(第三版).北京:华夏出版社,2001,173.
7 陈惠萍,曾彩虹.10594例肾活检病理资料分析.肾脏病与透析肾移植杂志,2000,9(6):501-509.
8 黄建萍,刘翠华.无症状肾小球性血尿63例临床与病理.实用儿科临床杂志,1999,14(4):192-194.
9 高远赋,刘光陵.小儿孤立性血尿的病理分析.肾脏病与透析肾移植杂志,2000,9(1):52-53.
10许瑞英,王培荣.血尿原因待查患儿的临床与病理分析.中国实用儿科杂志,2000,15(8):483-485.
11 Piqueras hi,White RH,Raafat F,et al.Renal biopsy diagnosis in children presenting with haematuria.Pediatr Nephrol,1998,12(5):386-391.
12 傅海东,刘爱民,王亚萍,等.91例无症状性血尿患儿临床和病理分析.浙江医学,2006,28(4):286-287.
13 张桂菊,沈颖.儿童单纯性血尿105例病理分析.北京医学,2004,26(4):254-256.
14 张镜人.慢性肾功能不全的证治探讨.上海中医药杂志,1982,(2):11-13
15 赵金锋.肾炎治疗宜存精去粗兼顾.肾炎尿毒症专辑.中医古籍出版社,1988.145.
16 刘志明.肾炎尿毒症专辑.中医古籍出版社,1988.66.
17 阮诗玮,郑敏麟,王智等.Igh肾病湿热证与肾穿刺活检病理组织关系的临床研究.中国中西医结合肾病杂志,2003,4(10):583-584.
18 陆鸿滨.原发性肾小球病湿热证100例分析.贵阳中医学院学报,1986,(2):30
19 余江毅,熊宁宁,余承惠,等.肾炎湿热病理的临床分析和实验研究.中国中西医结合杂志,1992,12(8):458-460.
20 徐大基.原发性肾小球疾病病理类型与中医证型分析.福建中医药,1999.30:18-19.
21 刘宏伟.原发性肾小球疾病湿热病理的临床研究.中医杂志,1996,37(11):688
22 王付民.慢性肾小球肾炎病理类型与中医分型相关性研究.辽宁中医杂志,1994,21(9):391-392.
23 陈香美,陈以平,李平,等.1016例IgA肾病患者中医证候的多中心流行病学调查及相关因素分析.中国中西医结合杂志,2006.(26)3:197-201.
24 胡仲仪,陈以平,查平,等.慢性肾小球肾炎病理分型与中医治疗分析.中国中西医结合杂志,1992,12(8):455-457.
25 叶景华.慢性肾炎中医药研究现状及展望.山东中医杂志,1994,13(1):11-13
26 沈庆法.肾脏病湿热证的研究.浙江中医学院学报,2000,24(1):39-42.
27 王海燕主编.肾脏病学(第二版).北京:人民卫生出版社,1996,648.
28 黎磊石,刘志红,陈惠萍,等.从临床角度认识系膜IgA肾病.中华肾脏病杂志,1992,8(2):106-110.
29 孙伟.第十二次全国中医肾病学术会议论文汇编,1997.
30 Tao K,Nicholls K,Rockman S,et al.Expression of complemento3receptors on neutrophils and erythrocytes in patients with IgA nephropathty.Clin Nephrol,1989,32:203:1990,34:103.
31 叶小玲,黄庆元,郑法雷,等.肾小球肾炎转归与细胞凋亡.国外医学,泌尿系统分册,1998,18(1):11.
32 张曦,赵从禄,等.原发性系膜增生性肾炎患者血小板活化状态的研究.中国中西医结合肾病杂志,2002,3(3):169-170.
33 聂莉芳,方芳.益气滋肾冲剂对IgA肾病小鼠蛋白尿及肾功能的影响.上海 中医药杂志,2000,34(3):45-47.
34 徐巍,张玉梅,吴茜,等.肾炎II号治疗IgA肾病血尿的实验研究.中国中医药科技,2002,9(1):26-27.
35 周家俊,高建东,何立群,等.固本通络冲剂治疗IgA肾病的实验研究.中国中西医结合肾病杂志,2003,(48):442-444.
36 余江毅,熊宁宁,余承惠,慢性肾病瘀血与湿热病理的临床和实验研究.辽宁中医杂志,1995,22(2):91-92.
37 刘宏伟.原发性肾小球疾病湿热病理的临床研究.中医杂志,1996,37(11):688-689
38 廖荣鑫,吴仕九,文小敏,等.脾胃湿热证热偏重、湿热并重型大鼠模型血液中胃动素(MTL)、胃泌素(GAS)的变化研究.浙江中医杂志,2005,40(4):171-173.
39 高清华,陈梁,吕文亮,等.清热化湿法对温病湿热证大鼠SP、SS水平影响的研究.湖北中医学院学报,2005,7(4):12-13.
40 廖礼兵,吴仕九,刘德传.清香散对湿热证大鼠中分子与巯基物质的影响.中国中医药科技,2002,9(1):44-44.
41 佟丽,陈江华.多因素所致温病温热证模型大鼠红细胞免疫功能的变化.中国免疫学杂志,1999,15(8):366-368.
42 吕文亮,柯裕枝,高清华,等.清热化湿法对温病湿热证大鼠抗利尿激素的影响.湖北中医学院学报,2005,7(4):7-9.
43 熊宁宁.家兔肾炎湿热证模型的实验研究.辽宁中医杂志,1991,18(4):42-43
44 朱辟疆,施荣华,刘永平.慢性肾小球疾病湿热证血浆及尿白介素-6的改变.浙江中西医结合杂志,1999,9(2):75-77.
45 Taniguchi Y,YoriokaN,Kumagai J,et al.Interleukin-6 localization and the prognosis of Igh nephropathy.Nephron JT-Nephron,1999,81(1):94-98.
1.王海燕主编.肾脏病学(第二版).北京:人民卫生出版社,1996,648。
2.钱铜荪主编.肾脏病学(第三版).北京:华夏出版社,2001,173。
3.Hawn CVZ,Janeway C.Histologic and serological sequences experimental hypersensitivity.J Exp Med,1947,85:571-590.
4.Germuth FG Jr,Taylor JJ,Siddiqui SY,et al.Immune complex disease.Ⅵ.Some determinants of the varieties of glomerular lesions in the chronic bovine serum albumin-rabbit system.Lab Invest,1977,37:162-169.
5.章友康.家兔慢性血清病所致系膜增殖型肾炎的改进探讨.中华肾脏病杂志,1986,2(1):2-4
6.贾慧,邹万忠.改良慢性血清病性大鼠系膜增生性肾炎模型的建立.肾脏病与透析肾移植杂志,1996,5(3):21-25.
7.Bagchus WM,Jeunink MF,Elema JD.The mesangium in anti-Thy-1nephritis.Influx of macrophages,mesangial cell hypercellularity,and macromolecular accumulation.Am J Pathol,1990,137:215-223.
8.Yamamoto T,et al.Anti-Thymocytc antibody induced mesangialytic nephritis.In:Hatano M,ed.Nephrology.Tokyo:Springer-Verlag,1991:1004.
9.刘志红,黎磊石,杨俊伟,等.抗Thy-1抗体与炎症因子诱发的系膜增殖性肾炎模型.中华肾脏病杂志,1993,9(2):95-96.
10.刘震,周树录,谭建三.大鼠系膜增生性肾模型的复制与改进.华西医科大学学报,1996,27(2):182-184.
11.黄怀鹏,陈志强,陈玉林,等.肾疏宁对大鼠系膜增生性肾炎的实验研究.中医药学刊,2003,21(2):271-272.
12.Miyawaki S,Muso E,Takeuchi E,et al.Selective breeding for high serum IgA levels from noninbred ddY mice:isolation of a strain with an early onset of glomerular Igh deposition.Nephron,1997,76:201-207.
13.Imai H,Nakamoto Y,Asakura K,et al.Spontaneous glomerular Igh deposition in ddY mice:an animal model of IgA nephritis.Kidney Int,1985,27:756-761.
14.hmore A,Roccatello D,Picciotto G,et al.Processing of Igh aggregates in a rat model of chronic liver disease.Clin Immunol Immunopathol,1997,84:107-114.
15.Melvin T,Burke B,Michael AF,et al.Experimental IgA nephropathy in bile duct ligated rats.Clin Immunol Immunopathol,1983,27:369-77.
16.Sato M,Ideura T,Koshikawa S.Experimental IgA nephropathy in mice.Lab Invest,1986,54:377-384.
17.Woodroffe AJ,Gormly AA,Clarkson AR,et al.Experimental cirrhosis and deposition of glomerular IgA immune complexes.Contrib Nephrol,1984,40:51-54.
18.邹万忠,韩可汉.补体在IgA肾病发生中的作用.中华肾脏病杂志,1992,8(6):333-336.
19.Rifai A,Small PA Jr,Teague PO,et al.Experimental IgA nephropathy.J Exp Med,1979,150:1161-1173.
20.Isaacs K,Miller F,Lane B.Experimental model for IgA nephropathy.Clin Immunol Immunopathol,1981,20:419-26.
21.Emancipator SN,Gallo GR,Lamm ME.Experimental IgA nephropathy induced by oral immunization.J Exp Med,1983,157:572-582.
22.章友康,王海燕.肝脏与IgA肾病的关系及其机制的探讨.北京医科大学学报,1988,20(4):257-260.
23.王丽,章友康,王海燕,等.肝脾和(或)胃肠粘膜免疫在肾小球系膜区IgA 沉积中的作用.中华内科杂志,1988,27(4):216-220.
24.刘志红,黎磊石,李莉.葡萄球菌肠毒素诱发的IgA肾病模型.中华肾脏病杂志,1989,5(1):6-10.
25.胡海翔,贾海骅.滋肾止血片对实验性IgA肾病大鼠治疗作用的实验研究.中国中医基础医学杂志,1999,5(1):39-44.
26.刘宏伟,卢景芬.滋肾止血片对实验性IgA肾病小鼠肾组织氧自由基的影响.中国中医基础医学杂志,1996,2:24-26.
27.胡顺金,曹恩泽,张敏,等.康肾止血颗粒剂对IgA肾病模型大鼠作用的实验研究.中医药临床杂志,2005,17(6):574-575.
28.刘志红,黎磊石.葡萄球菌肠毒素诱发的IgA肾病模型.中华肾脏病杂志,1989,5(1):6-10.
29.聂莉芳,方芳.益气滋肾冲剂对IgA肾病小鼠蛋白尿及肾功能的影响.上海中医药杂志,2000,34(3):45-47.
30.张远铮,白克敏,王宝琳.关于补体膜攻击复合物C56-9与实验性IgA肾病及人类IgA肾病可能致病作用的探讨.中华医学会第四次全国肾脏病学术会议论文汇编.1994,10
31.熊宁宁.家兔肾炎湿热证模型的实验研究.辽宁中医杂志,1991.18(4).42-43
32.李仕梅 主编.临床肾脏病学.上海:上海科技出版社,1986,254.
1 杨开清,林培政.清热化湿消瘀法对兔主动脉粥样硬化形成干预作用的超微结构研究.广州中医药大学学报,2006,2 3:318-321.
2 王新华.温病湿热证病理造型及实验研究.广州中医学院学报,1990,7:182-186.
3 吴仕九,杨运高.温病湿热证动物模型的研制及清祛湿法机理的探讨.中国中医药科技,1999,6:65-67.
4 郭明阳,阎翔.温病湿热证湿重于热动物模型的研究.成都中医药大学学报,2003,26:33-36.
5 廖荣鑫,吴仕九,文小敏,等.脾胃湿热证热偏重、湿热并重型大鼠模型血液中胃动素(MTL)、胃泌素(GAS)的变化研究.浙江中医杂志,2005,40:171-173.
6 阎翔,郭明阳.温病湿热证湿重于热动物模型舌的病理观察.安徽中医学院学报,2005,24:19-21.
7 高清华,陈梁,吕文亮,等.清热化湿法对温病湿热证大鼠SP、SS水平影响的研究.湖北中医学院学报,2005,7:12-13.
8 佟丽,陈江华.多因素所致温病温热证模型大鼠红细胞免疫功能的变化. 中国免疫学杂志,1999,15:366-368.
9 文彬,贺松其,吴仕九,等.清热祛湿方对肝纤维化大鼠肝组织SOD、MDA及超微结构的影响.上海中医药杂志,2005,39:56-58。
10吴仕九,杨运高,等.中医湿热证证候模型的应用研究.中医杂志,2001,42:553-555.
11 刘德传,吴仕九,等.清香散对湿热证模型大鼠—氧化氮含量的影响.中国中西医结合消化杂志,2001,9:131-132.
12 刘德传,吴仕九,等.微量元素、抗氧化剂与湿热证的相关性的研究.广东微量元素科学,2001,8:30-32.
13 廖礼兵,吴仕九,等.清香散对湿热证大鼠中分子与巯基物质的影响.中国中医药科技,2002,9:44-44.
14 吴仕九,廖礼兵,文小敏,等.温病湿热证湿热量化的相关性实验研究.中医杂志,2003,44:688-690.
15 吕文亮,柯裕枝,高清华,等.清热化湿法对温病湿热证大鼠抗利尿激素的影响.湖北中医学院学报,2005,7:7-9.