多廿烷醇抗动脉粥样硬化的分子机制研究

摘要

目的:探讨多廿烷醇抗动脉粥样硬化的分子机制.方法:采用腹腔注射维生素D3+高脂饮食喂养12周,建立大鼠动脉粥样硬化模型,同时使用多廿烷醇对其进行预干预.将40只SD大鼠随机平分成4组,为正常组、动脉粥样硬化组、阿托伐他汀组及多廿烷醇组.酶法(终点法/CHO-PAP Method)检测血清血脂水平,ELISA法检测血清炎症因子超敏C反应蛋白(hsCRP),取大鼠腹主动脉行电镜检查,采用Western blot法检测动脉粥样硬化斑块p38MAPK磷酸化的表达水平.结果:正常组可见完整内皮,动脉粥样硬化组大鼠腹主动脉有明显动脉粥样硬化形成,多廿烷醇组动脉粥样硬化程度较轻,大鼠血脂、血清hsCRP炎症因子及大鼠腹主动脉p38MAPK磷酸化表达量均在正常组最低,动脉粥样硬化组最高,多廿烷醇组居中(P＜0.05).结论:多廿烷醇除了具有调脂作用外,可对动脉粥样硬化大鼠血清炎症因子hs-CRP和p38MAPK磷酸化有一定抑制作用,p38MAPK磷酸化通路可能参与多廿烷醇抗动脉粥样硬化机制.%ObjectiverTo characterize the anti-atherosclerotic molecular mechanism of policosanol in atherosclerosis rat. Rat atherosclerosis model was prepared by intraperitoneal injection of vitamin D3 with high cholesterol diet for 12 weeks. Methods; Forty SD rats were randomly divided into four groups:the normal group,atherosclerosis (AS) group,atorvastatin group and policosanol group. Serum lipids and serum inflammatory cytokine hs-CRP were detected enzymalically(end-point method/CHO-PAP method) and ELJSA method, respectively. The atherosclerosis of the abdominal aorta was observed under an electron microscope. The expression of p-p38MAPK was analyzed by Western blot. Results;The normal group showed intact endothelium. AS formations were significantly greater in the AS group. The serum lipid levels,the content of serum inflammatory cytokines hs-CRP and the expression of p-p38MAPK in the policosanol group were between the AS group and the normal group,which were the highest in the AS group. Conclusion: Apart from its lipid-lowering effects,policosanol reduced the production of serum hs-CRP and inhibited the expression of p-p38MAPK in AS rats. The p38MAPK phosphorylation pathway may be involved in the anti-atherosclerosis molecular mechanism of policosanol in AS rats.