光甘草定通过p38/MAPK通路调控动脉粥样硬化模型兔动脉MLCK表达  

Regulation of glabridin on the expression of MLCK in endothelial cells through the pathway of p38/MAPK in the artery wall of atherosclerotic rabbits

作　　者：王淦娴 王怡[1] 丁俊丽[1] 丁延辉[1] 周青[1] 汪渊[1] 朱华庆[1] 

机构地区：[1]安徽医科大学分子生物学实验室生物化学与分子生物学教研室安徽省/省部共建教育部重要遗传病基因资源利用重点实验室,合肥230032

出　　处：《安徽医科大学学报》2017年第3期309-313,共5页Acta Universitatis Medicinalis Anhui

基　　金：国家自然科学基金(编号:81270372);安徽高校省级自然科学研究项目(编号:KJ2013Z127)

摘　　要：目的研究光甘草定能否通过p38/丝裂原活化蛋白激酶(MAPK)通路影响动脉粥样硬化(AS)兔模型主动脉内皮细胞肌球蛋白轻链激酶(MLCK)的表达。方法建立AS兔模型,将新西兰大耳白兔随机分为3组:正常对照组、高脂模型组、光甘草定组。正常对照组用正常饲料喂养;高脂模型组、光甘草定组用高脂饲料喂养,12周后分析血清中总胆固醇(TC)、三酰甘油(TG)成分的变化,通过苏木精-伊红(HE)染色分析兔动脉壁形态结构变化;免疫组织化学方法观察兔模型主动脉内膜MLCK的分布和表达;Western blot分析兔动脉内膜MLCK水平及p38蛋白磷酸化变化。结果成功建立AS兔模型,在给予高脂饮食12周以后,与正常对照组相比,血清中TC增高(P<0.05),TG有所增加,但差异无统计学意义;大体标本观察到大量兔动脉粥样斑块形成,HE染色显示高脂模型组兔主动脉血管内皮细胞间隙明显增大并伴有大量泡沫细胞,内膜增厚明显;免疫组化显示主动脉内膜MLCK表达量增多;Western blot显示动脉p38磷酸化水平增强(P<0.05)。而加喂光甘草定后,血管内膜病变程度有所下降,MLCK表达有所下降,动脉p38磷酸化水平有所下降(P<0.05)。结论光甘草定可能通过p38/MAPK通路影响AS兔模型主动脉内皮细胞MLCK的表达。Objective To discuss whether myosin light chain kinase （MLCK） in arterial endothelial cells was accommodated by glabridin through the pathway of p38/MAPK on atherosclerosis （AS） model rabbit. Methods The AS model rabbit was set up and New Zealand white rabbits were randomly divided into three groups：normal group, high fat model group, glabridin group. The changes of serum lipid components was analyzed in model rabbit. The uhrastructural changes of rabbit arterial wall was observed through by hematoxylin-eosin staining （ HE ）. The distribution and expression of MLCK in rabbit arterial intima was measured by immunohistochemistry. The changes of MLCK and p38 phosphorylation in endothelial cells was surveyed by Western blot. Results The establishment of AS rabbit model was successful. After being fed up with the high fat diet for 12 weeks, the atherosclerotic plaques were observed clearly. And compared with the normal control, HE staining showed that the gap between the endothe- lial cells was gradually increased, and a large number of foam cells were formatted. The expression of MLCK and the expression of p38 phosphorylation was enhanced in the rabbit artery tissue. After glabridin was added into the high fat food, the expression of the MLCK and the p38 phosphorylation in the artery tissue were decreased. The level of aortic intimal lesion was certainly lessend. Conclusion Glabridin may regulate the expression of MLCK in endothe- lial cell of AS model of rabbit artery by the pathway of p38/MAPK.

关 键 词：动脉粥样硬化 肌球蛋白轻链激酶 光甘草定 

分 类 号：R972.6[医药卫生—药品]