黄芩苷对动脉粥样硬化家兔的保护作用及其机制

Effects and possible mechanisms of baicalin on the atherosclerosis rabbits

目的:探讨黄芩苷对动脉粥样硬化(AS)家兔的保护作用及可能机制。方法:新西兰白兔30只,随机分为正常组、模型组、黄芩苷治疗组(300mg/kg)、黄芩苷预防组(100mg/kg)、阳性药(辛伐他汀)对照组,每组6只。酶法测定各组血清及肝脏中TC、TG、低密度脂蛋白(LDL)、高密度脂蛋白含量,主动脉苏丹Ⅳ染色测AS斑块面积/总面积,HE染色观察主动脉及肝脏形态学改变。ELASA方法测血清中肿瘤坏死因子(TNF-α)、白细胞介素-1β(IL-1β)、脂联素(Adiponectin)的水平。免疫组化法检测主动脉弓处的NF-κB的表达。结果:黄芩苷治疗组、黄芩苷预防组、阳性药对照组主动脉粥样硬化斑块面积小于模型组(P<0.01),黄芩苷治疗组、黄芩苷预防组、阳性药对照组血清及肝脏中TC、LDL水平较模型组明显降低(P<0.01),黄芩苷治疗组、黄芩苷预防组血清中TNF-α、IL-1β和脂联素水平较模型组明显降低(P<0.01,P<0.05),黄芩苷治疗组、黄芩苷预防组主动脉壁上NF-κB的表达低于模型组(P<0.01)。结论:黄芩苷通过升高脂联素、下调NF-κB抑制炎症反应及调节血脂两个方面对AS起保护作用,这可能是其抑制AS的形成及发展的重要机制之一。

AIM： To investigate the effects and possible mechanisms of baicalin on the atherosclerosis rabbits. METIHODS： Thirty healthy New Zealand white rabbits were divided randomly into five groups： normal control group （A group, n =6） and fed with normal diet, atherosclerosis model group （ B group, n =6）, baicalin thempic group（C group, n = 6）, bacalin preventive group（D group, n = 6）, and positive control group（ E group, n = 6）, the last four groups fed with hypercholesterol diet for 12 weeks. Treated with bacalin 300 mg/（kg· d）, and simvastatin 5 mg/ （kg· d） additionally for 2 weeks in C and E group respectively from the tenth week. Treat with bacahn 100 mg/（kg·d）for 12 weeks in D group. Serum lipids and liver lipids were detected with standard enzymatic assays. Atherosclerotic plaque/intima size ratio of area and NF-kB content in blood vessel tissue were examined. Enzyme-linked immunosorbent assay （ELISA） was employed to monitor the levels of serum TNF-α, IL-1β and Adiponectin. RESULTS： Atherosclerotic plaque/intima size ratio of area decreased in C, D and E group than in B group（ P 〈 0.01 ）. The levels of Blood lipids, liver lipids decreased in C, D and E group than in B group（ P 〈 0.01 ）. Serum TNF-α, IL- 1β, and adiponectin decreased in C and D group than in B group（ P 〈 0.01, P 〈 0.05）. The NF-kB activity in C and D group were lower than B group（ P 〈 0.01 ）. CONCLUSION： Baicalin improve atherosclerosis not only by decreasing blood lipids, but also by anti-inflammation through increasing serum levels of adiponectin, decreasing activity of NF-kB in atherosclerotic focus and serum levels of TNF-α, IL-1β.