黄芪甲苷对血管紧张素Ⅱ诱导肾小球系膜细胞增殖及炎症因子表达的影响

Effects of astragaloside-Ⅳ on the expression of inflammatory factor and proliferation of glomerular mesangial cells induced by angiotensin Ⅱ

目的:研究黄芪甲苷(As-Ⅳ)对血管紧张素Ⅱ(AngⅡ)诱导大鼠肾小球系膜细胞(GMCs)增殖及炎症因子表达的影响。方法:采用10^(-6)mol/L的AngⅡ刺激GMCs增殖,同时分别加入25,50,100μmol/L的As-Ⅳ对GMCs作用48 h,运用MTT法检测各组细胞增殖状况;流式细胞术观察GMCs中细胞内活性氧(ROS)水平变化;ELISA法检测细胞上清液中单核细胞趋化蛋白-1(MCP-1)的含量; Western blot法检测细胞中转化生长因子β1(TGF-β1)蛋白的表达。结果:与AngⅡ刺激组相比,As-Ⅳ干预显著抑制GMCs细胞增殖,减少细胞内ROS水平,抑制MCP-1及TGF-β1的表达。结论:As-Ⅳ对于AngⅡ诱导GMCs的增殖具有抑制作用,且能降低相关炎症因子的表达。

Objective: To study the effects of astragaloside-Ⅳ( As-Ⅳ) on the expression of inflammatory factor and proliferation of glomerular mesangial cells( GMCs) induced by angiotensin Ⅱ( Ang Ⅱ). Methods: The in vitro model of diabetic nephropathy( DN) was mimic by angiotensin Ⅱ( 10-6 mol/L) inducing GMCs injury. Then the GMCs were treated with As-Ⅳ at different concentrations( 25,50,100 μmol/L) for 48 hours. The proliferation of GMCs was detected by MTT. The level of reactive oxidative species( ROS)was measured by flow cytometry. The expression of monocyte chemoattractant protein-1( MCP-1) protein in supernatant was detected by enzyme-linked immunosorbent assay( ELISA). The expression of transforming growth factor-β1( TGF-β1) in GMCs was measured by Western blot. Results: Compared with model group,the proliferation of GMCs was inhibited in As-Ⅳ group. As-Ⅳ decreased the level of intercellular ROS,down-regulated the secretion of MCP-1 and the expression of TGF-β1 proteins. Conclusion: As-Ⅳ could inhibit cell proliferation and inflammatory factors expression on GMCs induced by AngⅡ.