竹节参皂苷IVa甲酯对血管紧张素Ⅱ诱导的血管平滑肌细胞增殖影响及机制研究  

Effects and mechanism of chikusetsu saponin iva methyl to VSMCs proliferation

作　　者：杨冬梅[1] 聂娟[2] 孙四玉 邱飞[1] 刘杨[3] 王炜[3] 熊国祚[4] 廖端芳[1] 庹勤慧[1] 

机构地区：[1]湖南中医药大学药理教研室 [2]湖南中医药大学医学院血管生物学实验室 [3]湖南中医药大学中药民族药物创新与发展实验室 [4]南华大学第二附属医院普外科

出　　处：《中国临床药理学与治疗学》2016年第8期873-877,共5页Chinese Journal of Clinical Pharmacology and Therapeutics

基　　金：国家自然科学基金项目(31371161;81673722);湖南省自然科学基金项目(14JJ1024;2015JJ2117)

摘　　要：目的:探讨竹节参皂苷IVa甲酯(chikusetsu saponin iva methyl,CSIM)对血管紧张素II(angiotensin,Ang-II)刺激的血管平滑肌细胞(vascular smooth muscle cells,VSMCs)增殖的影响及机制研究。方法:以大鼠血管平滑肌细胞为实验对象,建立Ang-II刺激的VSMCs增殖模型。MTT法检测CSIM对VSMCs的毒性;CCK-8法、Brd U法检测CSIM对VSMCs增殖的影响,划痕实验检测CSIM对VSMCs迁移力的影响,免疫蛋白印迹法检测PTEN、NF-κB蛋白表达水平。结果:3μmol/L的CSIM可显著抑制Ang-II诱导的VSMCs增殖(P<0.05)与迁移(P<0.05),并伴随着PTEN蛋白的明显上调(P<0.05)及NF-κB蛋白表达的显著性降低(P<0.05)。结论:CSIM抑制Ang-II诱导的VSMCs增殖与迁移,其机制可能与上调PTEN蛋白,降低NF-κB蛋白表达有关。AIM： To observe the effects and mechanism of chikusetsu saponin iva methyl to vascular smooth muscle cells（ VSMCs） proliferation.METHODS： VSMCs was cultured in vitro and the cell proliferation model was established by Ang-II.The VSMCs toxicity were determined by MTT assay,the proliferation of VSMCs was detected by CCK-8and Brd U assay,the VSMCs migration distance was detected by wound-healing assay,the PTEN,NF-κB protein expression was determined by Western blot assay. RESULTS： 3 μmol / L of chikusetsu saponin iva methyl significantly inhibited the proliferation and migration of Ang-II-induced VSMCs（ P〈0. 05）,increased PTEN protein expression（ P〈0. 05）,reduced NF-κB protein expression（ P〈0. 05）. CONCLUSION： Chikusetsu saponin iva methyl can inhibit the proliferation and migration of Ang-II induced VSMCs,which may be related to regulating PTEN protein,reducing NF-κB protein expression.

关 键 词：竹节参皂苷IVa甲酯 血管平滑肌细胞 增殖 作用机制 

分 类 号：R965.2[医药卫生—药理学]