血脂康通过减少CD68、脂质沉积和新生血管生成并增加α肌动蛋白和胶原稳定斑块  

Xuezhikang stabilize atherosclerotic plaque through both reducing CD68,lipid accumulation,neovascularization and increasingα-actin and collagen

作　　者：李敏[1] 秦龙 宋卫东[2] 王玲玲 李锦师[1] 白青科[1] Li Min;Qin Long;Song Weidong;Wang lingling;Li Jinshi;Bai Qingke(Department of Neurology,the Shanghai Pudong New Area People's Hospital,Shanghai 201200,China)

机构地区：[1]浦东新区人民医院神经内科,上海201200 [2]浦东新区人民医院急诊科,上海201200

出　　处：《脑与神经疾病杂志》2022年第1期1-5,共5页Journal of Brain and Nervous Diseases

基　　金：浦东新区卫生健康委员会临床特色学科建设基金(PWYst2018-01);上海市浦东新区卫生健康委员会面上科技项目(PW2021A-60);浦东新区卫生和计划生育委员会学科群建设基金(PWZxq2017-02)。

摘　　要：目的研究血脂康对动脉硬化斑块稳定性的作用及机制。方法将小鼠分为对照组和血脂康组。染色斑块、巨噬细胞CD68、脂肪、新生血管CD31、血管内皮生长因子(vascular endothelial growth factor,VEGF)、血管生成素1(recombinant angiopoietin-1,ANGPT-1)、血管生成素2(recombinant angiopoietin-2,ANGPT-2)、平滑肌α肌动蛋白和胶原。结果血脂康组斑块、CD68、脂肪、CD31和VEGF减少(P<0.05),而ANGPT-1、平滑肌α肌动蛋白和胶原增加。结论血脂康通过减少斑块内巨噬细胞、脂质、新生血管生成并增加平滑肌α肌动蛋白和胶原稳定动脉硬化斑块。Objective To explore the effect and the mechanism of Xuezhikang on atherosclerotic plaque stabilization.Method Apolipoprotein E deficient(apoE-/-)mice were divided into two groups at random:blank control group and Xuezhikang group.Mice were subjected to the vulnerable plaque model by partial ligation method and then fed control and Xuezhikang.We prepared frozen section and dyed plaque,macrophage marker CD68,lipid,CD31,VEGF,ANGPT-1,ANGPT-2,α-actin and collagen.Results Xuezhikang group showed markedly decrease in plaque area,CD68,lipid,CD31 and VEGF(P<0.05),while significantly increase in ANGPT-1.α-actin and collagen.Conclusion Xuezhikang reduce plaque area through decreasing macrophage,lipid accumulation,neovascularization and increasingα-actin and collagen,to stabilize atherosclerotic plaque.

关 键 词：血脂康 巨噬细胞 新生血管生成 Α肌动蛋白 胶原 

分 类 号：R743[医药卫生—神经病学与精神病学]