柴白温胆汤对动脉粥样硬化大鼠氧化应激和炎症因子表达的影响
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摘要
目的:探讨柴白温胆汤对动脉粥样硬化(Atherosclerosis,AS)大鼠氧化应激和炎症因子表达的影响。方法:将45只大鼠分为对照组、模型组、他汀组和柴白温胆汤组,用维生素D3联合高脂饲料喂养8周建立AS模型,并给予相应的药物灌胃4周。第12周检测各组大鼠的体质量、总胆固醇(Total cholesterol,TC)、甘油三酯(Triglyceride,TG)、低密度脂蛋白胆固醇(Low density lipoprotein cholesterol,LDL-C)、高密度脂蛋白胆固醇(High density lipoprotein cholesterol,HDL-C)、核转录因子(Nuclear transcription factor-κB,NF-κB)、肿瘤坏死因子-α(Tumor necrosis factor-α,TNF-α)、白细胞介素-6 (Interleukin-6,IL-6)、白细胞介素-1β(Interleukin-1β,IL-1β)、超敏C-反应蛋白(Hypersensitive C-reactive protein,hs-CRP)、超氧化物歧化酶(Superoxide dismutase,SOD)、谷胱甘肽过氧化物酶(Glutathione peroxidase,GSH-Px)、过氧化氢酶(Catalase,CAT)、丙二醛(Malonaldehyde,MDA)及活性氧簇(Reactive oxygen species,ROS)水平。结果:与对照组比较,模型组大鼠体质量、TC、TG、LDL-C、NF-κB、TNF-α、IL-6、IL-1β、hs-CRP、MDA、ROS水平明显升高(P <0.05),HDL-C、SOD、GSH-Px、CAT水平明显降低(P <0.05)。与模型组比较,柴白温胆汤组和他汀组大鼠体质量、TC、TG、LDL-C、NF-κB、TNF-α、IL-6、IL-1β、hsCRP、MDA、ROS水平明显降低(P <0.05),HDL-C、SOD、GSH-Px、CAT水平明显升高(P <0.05)。与他汀组比较,柴白温胆汤组各检测指标差异无统计学意义(P> 0.05)。结论:柴白温胆汤可能通过抑制NF-κB、TNF-α、IL-6、IL-1β、hs-CRP、MDA、ROS的表达,促进HDL-C、SOD、GSH-Px、CAT的表达来防治AS。
Objective: To explore the effect of Chaibai Wendan tang on oxidative stress and expression of inflammatory factors in rats with atherosclerosis. Methods:45 rats were divided into the control group,the model group,the statin group and the Chaibai Wendan tang group randomly,10 rats in each group. The model of rats with AS was established by feeding them with vitamin D3 combined with high fat feed for 8 weeks and giving them corresponding medicine via gavage for 4 weeks. In the 12~(th) week,detected the levels of body mass,total cholesterol(TC),triglyceride(TG),low density lipoprotein cholesterol(LDL-C), high density lipoprotein cholesterol(HDL-C), nuclear transcription factor-κB(NF-κB), tumor necrosis factor-α(TNF-α), interleukin-6(IL-6), interleukin-1β(IL-1β), hypersensitive C-reactive protein(hs-CRP), superoxide dismutase(SOD),glutathione peroxidase(GSH-Px),catalase(CAT),malonaldehyde(MDA) and reactive oxygen species(ROS)of rats in each group. Results: Comparing with the control group, the levels of body mass, TC, TG, LDL-C, NF-κB,TNF-α,IL-6,IL-1β,hs-CRP,MDA and ROS of rats in the model group were significantly increased(P < 0.05),and the levels of HDL-C, SOD, GSH-Px and CAT were significantly decreased(P < 0.05). Comparing with the model group, the levels of body mass, TC, TG, LDL-C, NF-κB, TNF-α, IL-6, IL-1β, hs-CRP, MDA and ROS of rats in the statin group and the Chaibai Wendan tang group were significantly decreased(P < 0.05),and the levels of HDL-C,SOD,GSH-Px and CAT were significantly increased(P < 0.05). Comparing with the statin group,there was no significant difference being found in each index in the Chaibai Wendan tang group(P > 0.05). Conclusion:Chaibai Wendan tang may prevent and treat AS by means of inhibiting the expression of NF-κB, TNF-α, IL-6, IL-1β, hs-CRP, MDA and ROS and promoting the expression of HDL-C,SOD,GSH-Px and CAT.
Objective: To explore the effect of Chaibai Wendan tang on oxidative stress and expression of inflammatory factors in rats with atherosclerosis. Methods:45 rats were divided into the control group,the model group,the statin group and the Chaibai Wendan tang group randomly,10 rats in each group. The model of rats with AS was established by feeding them with vitamin D3 combined with high fat feed for 8 weeks and giving them corresponding medicine via gavage for 4 weeks. In the 12~(th) week,detected the levels of body mass,total cholesterol(TC),triglyceride(TG),low density lipoprotein cholesterol(LDL-C), high density lipoprotein cholesterol(HDL-C), nuclear transcription factor-κB(NF-κB), tumor necrosis factor-α(TNF-α), interleukin-6(IL-6), interleukin-1β(IL-1β), hypersensitive C-reactive protein(hs-CRP), superoxide dismutase(SOD),glutathione peroxidase(GSH-Px),catalase(CAT),malonaldehyde(MDA) and reactive oxygen species(ROS)of rats in each group. Results: Comparing with the control group, the levels of body mass, TC, TG, LDL-C, NF-κB,TNF-α,IL-6,IL-1β,hs-CRP,MDA and ROS of rats in the model group were significantly increased(P < 0.05),and the levels of HDL-C, SOD, GSH-Px and CAT were significantly decreased(P < 0.05). Comparing with the model group, the levels of body mass, TC, TG, LDL-C, NF-κB, TNF-α, IL-6, IL-1β, hs-CRP, MDA and ROS of rats in the statin group and the Chaibai Wendan tang group were significantly decreased(P < 0.05),and the levels of HDL-C,SOD,GSH-Px and CAT were significantly increased(P < 0.05). Comparing with the statin group,there was no significant difference being found in each index in the Chaibai Wendan tang group(P > 0.05). Conclusion:Chaibai Wendan tang may prevent and treat AS by means of inhibiting the expression of NF-κB, TNF-α, IL-6, IL-1β, hs-CRP, MDA and ROS and promoting the expression of HDL-C,SOD,GSH-Px and CAT.
引文
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[16]FUJIMOTO H,KOBAYASHI H,OHNO M.Age-induced reduction in mitochondrial manganese superoxide dismutase activity and tolerance of macrophages against apoptosis induced by oxidized low density lipoprotein[J].Circulation Journal,2010,74(2):353-360.
[17]LI X,ZHAO L,YUE L,et al.Evidence for the protective effects of curcumin against oxyhemoglobin-induced injury in rat cortical neurons[J].Brain Research Bulletin,2015,120:34-40.
[2]XI B,LIU F,HAO Y,et al.The growing burden of cardiovascular diseases in China[J].International Journal of Cardiology,2014,174(3):736-737.
[3]KNOBLER H,BITZUR R,GAVISH D,et al.Prevention and treatment of atherosclerosis and cardiovascular diseases[J].Harefuah,2012,151(5):281.
[4]HERRINGTON W,LACEY B,SHERLIKER P,et al.Epidemiology of Atherosclerosis and the Potential to Reduce the Global Burden of Atherothrombotic Disease[J].Circulation Research,2016,118(4):535.
[5]LIBBY P.Inflammation in atherosclerosis[J].Arteriosclerosis Thrombosis&Vascular Biology,2012,32(9):2045-2051.
[6]LI H,HORKE S,F魻RSTERMANN U.Vascular oxidative stress,nitric oxide and atherosclerosis[J].Atherosclerosis,2014,237(1):208-219.
[7]曹洪涛.心血管疾病防治的中医药优势[J].西部中医药,2016,29(10):139-141.
[8]刘炜枫,赵帅,陈伯钧,等.LXR m RNA在动脉粥样硬化兔中的表达变化[J].海南医学,2016,27(15):2413-2415.
[9]GALKINA E,LEY K.Immune and Inflammatory Mechanisms of Atherosclerosis[J].Annual Review of Immunology,2008,27(1):165-197.
[10]KANG L,CHING D,FU S L,et al.Micro RNA-146a suppression of NF-κB-driven monocyte/macrophage activation and atherosclerosis is regulated by cellular Apo E expression[J].Angiogenesis,2015,17(4):939.
[11]SBARSI I,FALCONE C,BOIOCCHI C,et al.Inflammation and atherosclerosis:the role of TNF and TNFreceptors polymorphisms in coronary artery disease[J].Int JImmunopathol Pharmacol,2007,20(1):145-154.
[12]LEGEIN B,TEMMERMAN L,BIESSEN E A,et al.Inflammation and immune system interactions in atherosclerosis[J].Cellular&Molecular Life Sciences,2013,70(20):3847-3869.
[13]NISHIDA M,MORIYAMA T,ISHII K,et al.Effects of IL-6,adiponectin,CRP and metabolic syndrome on subclinical atherosclerosis[J].Clinica Chimica Acta,2007,384(1-2):99.
[14]PAFFEN E,DEMAAT M P.C-reactive protein in atherosclerosis:A causal factor?[J].Cardiovascular Research,2006,71(1):30-39.
[15]BRADLEY R L,FISHER F F,MARATOS-FLIER E.Dietary fatty acids differentially regulate production of TNF-alpha and IL-10 by murine 3T3-L1 adipocytes[J].Obesity,2008,16(5):938-944.
[16]FUJIMOTO H,KOBAYASHI H,OHNO M.Age-induced reduction in mitochondrial manganese superoxide dismutase activity and tolerance of macrophages against apoptosis induced by oxidized low density lipoprotein[J].Circulation Journal,2010,74(2):353-360.
[17]LI X,ZHAO L,YUE L,et al.Evidence for the protective effects of curcumin against oxyhemoglobin-induced injury in rat cortical neurons[J].Brain Research Bulletin,2015,120:34-40.