目的:研究灵仙新苷(clematichinenoside AR)调节血脂及抗动脉粥样硬化的作用.方法:采用高脂饲料喂饲和腹腔注射维生素D3结合腹腔注射LPS建立大鼠动脉粥样硬化模型,造模成功后灌胃给予高、中、低剂量的AR(32,16,8 mg·kg-1·d-1),8周后测定大鼠血清胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白-胆固醇(HDL-C)、低密度脂蛋白-胆固醇(LDL-C)、肿瘤坏死因子(TNF-α)、一氧化氮(NO)及诱导型一氧化氮合酶(iNOS)；取其胸主动脉进行油红O染色,观察大鼠胸主动脉内膜脂质沉积情况；取肝脏进行常规HE染色,观察肝脏病变.结果:AR高、中剂量组能显著降低高血脂症大鼠血清TC,TG,LDL-C,TNF-α,NO水平和iNOS活力,升高HDL-C水平,差异具有统计学意义(P＜0.05).同时,AR能减少主动脉内皮脂质沉积,改善肝脏的脂肪变性和炎症细胞浸润.结论:AR具有调节血脂,减轻动脉粥样硬化发生和发展的作用,该作用与其调节NO及其合酶的形成和表达相关.%Objective: To examine whether clematichinenoside (AR) affects blood lipid metabolism, atherosclerosis and hepatic lipogenesis in rats. Methods: Firstly, hypercholesterolemia in rats was induced by feeding a high-fat with intraperitoneal injection of vitamin D3 and LPS. Then the rats were intragastrically administered with AR (32, 16 and 8 mg·kg-1· d-1). The levels of TC , TG, LDL-C , HDL-C , TNF-α, NO and iNOS in serum were analyzed. The lipidoses of aorta was detected by oil red 0 staining in frozen sections. Finally the pathological changes in liver lipogenesis were examined. Results: AR significantly reduced the levels of TC, TG, LDL-C, TNF-α, NO and iNOS, and increased the levels of HDL-C as compared with control hypercholesterolemic rats. The oil red 0 staining in frozen sections showed that AR decreased the lipidoses of aorta. Pathological examination showed that AR attenuated hepatic cell steatosis and inflammatory cell recruiting. Conclusion: AR can modify lipid metabolism, decrease the lipidoses of aorta and attenuate hepatic lipogenesis in hypercholesterolemic rats.
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