熊果酸抑制大鼠血管平滑肌细胞增殖的作用及其机制

Inhibitory effects and mechanism of ursolic acid on the proliferation of rat aortic smooth muscle cells

目的:研究熊果酸(UA)对大鼠血管平滑肌细胞(VSMC)增殖的抑制作用,并探讨其对p38MAPK信号通路的影响。方法:高糖(葡萄糖,25mmol/L)诱导VSMC增殖为模型,MTT法检测UA对细胞增殖的影响,Cell-based ELISA测定UA对p38MAPK磷酸化水平变化,采用SABC免疫组化法测定UA对细胞c-fos蛋白表达水平的影响。结果:UA(20,40μmol/L)能抑制高糖诱导的VSMC增殖作用(P<0.05)。UA组p38MAPK的磷酸化水平明显低于葡萄糖模型组(P<0.05),且c-fos的蛋白表达水平较模型组也明显降低。结论:UA可以抑制大鼠VSMC增殖,此作用可能与其抑制p38MAPK信号传导通路激活,从而下调c-fos蛋白表达有关。

Aim：To observe the effect of ursolic acid（UA）on the proliferation of rat vascular smooth muscle cell（VSMC）induced by high-level glucose and explore its relationship with p38MAPK signal transduction pathway.Methods：The proliferation of VSMC induced by high-level glucose（25 mmol/L glucose）was adopted as model,the inhibition of UA on the proliferation of VSMC was measured by MTT assay,and the expression levels of phospho-p38MAPK was detected by cell-based ELISA as well as the expression of c-fos protein was examined by SABC method.Results：UA（20 μmol/L and 40 μmol/L）inhibited glucose-induced proliferation of VSMC（P0.05）.Compared with the group subjected to glucose induction,UA decreased the expression levels of phosphorylated p38MAPK（P0.05）,and also inhibited c-fos expression.Conclusion：UA suppressed glucose induced proliferation of VSMC,which might be related to the suppression of the activation of p38MAPK signal transduction pathway,and thereby down-regulated c-fos expression.