绞股蓝总苷对高脂血症大鼠血管平滑肌细胞表型的影响  

Effects of Gypenosiedes on Vascular Smooth Muscle Cells Phenotype in Hyperlipidemic Rats

作　　者：束波[1] 刘志江[2] 钱民章[1] 

机构地区：[1]遵义医学院生物化学与分子生物学教研室 [2]遵义医学院第一附属医院心内科,遵义563003

出　　处：《天然产物研究与开发》2017年第2期217-223,共7页Natural Product Research and Development

基　　金：贵州省中医药管理局中医药;民族医药科学技术研究课题(QZYY-2015-152);遵义医学院2012招标课题(F-613)

摘　　要：研究绞股蓝总苷对高脂诱导的大鼠血管平滑肌细胞表型的影响及可能的分子机制。采用高脂饲料喂饲建立高脂大鼠模型,观察绞股蓝总苷对血脂各成分的影响,血管平滑肌细胞超微结构及血管表型标志物表达的影响。结果显示,绞股蓝总苷能降低大鼠血脂水平并抑制血管平滑肌细胞超微结构发生去分化表型改变;增加高脂大鼠动脉分化标志蛋白SM-actin的表达,降低细胞增殖蛋白PCNA的表达。说明绞股蓝总苷能有效抑制高脂诱导的大鼠平滑肌细胞去分化,机制可能与抑制MCPIP1的表达有关。The aim of this study was to investigate the functions and regulatory pathway of gypenosiedes（ GP） on vascular smooth muscle cells（ VSMCs） phenotype in hyperlipidemic rats. Hyperlipidemic rats model were established by feeding rats with high-fat diet. Blood lipid levels were detected in all groups. The ultrastructure of VSMCs was detected by transmission electron microscope. The expression of smooth muscle actin（ SM-actin）,proliferating cell nuclear antigen（ PCNA） and monocyte chemotactic protein-1 induced protein（ MCPIP1） in VSMCs were determined by using immunohistochemistry staining and Western blot methods. The experimental results showed that GP can decrease the blood lipids levels. GP effectively attenuated dedifferentiated changes of VMSCs ultrastructure and increased the expression of SM-actin. The expressions of PCNA and MCPIP1 in VSMCs were both decreased in GP group. These results demonstrate a novel protection role of GP in VSMCs dedifferentiation by inhibiting MCPIP1 expression.

关 键 词：绞股蓝总苷 血管平滑肌细胞 表型 单核细胞趋化蛋白-1诱导蛋白1 

分 类 号：R281.5[医药卫生—中药学]