芪丹煎干预兔动脉粥样斑块形成的分子机制  

MOLECULAR MECHANISMS OF THE INTERVENTION OF QIDANJIAN IN RABBIT ATHEROSCLEROTIC PLAQUE

作　　者：周玲生[1] 包东武[1] 

机构地区：[1]河南南阳医学高等专科学校.南阳 473000

出　　处：《现代预防医学》2010年第7期1395-1397,共3页Modern Preventive Medicine

摘　　要：[目的]探讨芪丹煎对家兔动脉粥样硬化干预作用的分子机制。[方法]建立家兔动脉粥样硬化模型,比较对照组、高脂组、西药组和芪丹煎组动脉粥样硬化斑块形成的变化;检测各组血清血脂水平;免疫组化结合RT-PCR法分析Bcl-2、Bax在粥样硬化斑块中的表达。[结果]芪丹煎组血脂水平和动脉粥样斑块面积低于高脂组(P﹤0.01);免疫组化显示,高脂组Bcl-2、Bax表达与正常组差异有统计学意义。而芪丹煎的干预可以调节Bax/Bcl-2阳性细胞表达率。[结论]芪丹煎可抑制动脉粥样硬化斑块的形成;调节Bcl-2/Bax表达可能是抗动脉粥样硬化的机制之一。[Objective] To investigate molecular mechanisms of the intervention of Qidanjian in rabbit atheroselerotic plaque, [ Methods] By Establishing rabbit atherosclerosis model, changes oft atherosclerofic plaque formation were compared among the control group, high-fat group, western medicine group and the Qidanjian group; serum lipid levels were detect in each group; the expressions of Bcl-2 and Bax in the atherosclerofic plaque were tested by immunohistochemistry with RT-PCR analysis. [ Results] Lipid levels and atherosclerotic plaque area in Qidanjian were lower than those of the high-fat group （P 0.01 ） ; Immunohistochemistry showed that Bcl-2 and Bax expressions of High-fat group had significantly difference compared with the control group, while the intervention of Qidanjian may adjust the expression rate of Ba.x/Bcl-2 positive cell. [Corlclu, sion ] Qidanjian inhibit atherosclerotic plaque formation; regulating Bel-2/Bax expression is possibly one of anti-atheroselerosis mechanisms.

关 键 词：动脉粥样硬化 蓖丹煎:Bax/Bcl-2 

分 类 号：R543[医药卫生—心血管疾病]