黄芩苷对动脉粥样硬化家兔的保护作用及其机制

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，T、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。EIASA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（Adiponeetin）的水平。免疫组化法检测主动脉弓处的NF-kB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—kB的表达低于模型组（P〈02．01）。结论：黄芩苷通过升高脂联素、下调NF—kB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。

Effects and possible mechanisms of baicalin on the atherosclerosis rabbits

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.