摘要
目的观察黄芪注射液对血管紧张素Ⅱ(AngⅡ)诱导的心肌成纤维细胞分泌转化生长因子(TGF-β1)的影响。方法体外培养乳鼠心脏成纤维细胞并制成单细胞悬液,分为对照组,黄芪低、中、高剂量组,AngⅡ组,AngⅡ联合黄芪低、中、高剂量组,分别加入50、100、200 mg/ml黄芪注射液,以及10-7 mol/L AngⅡ,共同培育2 d。用四甲基偶氮哇盐法测定各组细胞增殖情况,ELISA法测定培养上清TGF-β1分泌情况。结果各组间细胞增殖率差异有统计学意义(F=71.84,P=0.000);AngⅡ组的细胞增殖率明显升高,与其余各组比较均有统计学意义(P均<0.05);AngⅡ联合黄芪后,随着黄芪剂量的逐渐增加,细胞增殖率逐渐下降,差异均有统计学意义(P<0.05)。各组间TGF-β1分泌量差异也有统计学意义(F=786.81,P=0.000);黄芪低、中、高剂量组的TGF-β1分泌量均低于对照组,差异有统计学意义(P均<0.05);AngⅡ组的TGF-β1分泌量为各组中最高,与其余各组比较均有统计学意义(P均<0.05);AngⅡ联合黄芪后,随着黄芪剂量的逐渐增加,TGF-β1分泌量逐渐下降,差异均有统计学意义(P<0.05)。结论 AngⅡ可刺激心肌成纤维细胞增殖,促进心肌成纤维细胞分泌TGF-β1,而黄芪注射液可明显抑制AngⅡ诱导心肌成纤维细胞的增殖作用,并且减少心肌成纤维细胞分泌TGF-β1。
Objective To observe the effect of Astragalus membranaous on angiotensin Ⅱ(Ang Ⅱ)-induced transforming growth factor β1(TGF-β1) production of cardiac fibroblasts.Methods Cardiac fibroblasts were cultured in vitro.Cells were allocated into 3 groups:control group,Astragalus membranaous groups(50,100,200 mg/ml),Ang II group(10-7 mol/L) and Ang Ⅱ /Astragalus membranaous groups(50,100,200 mg/ml).The proliferation of each group was tested by methyl thiazolyl tetrazolium method.TGF-β1 was measured by ELISA.Results The proliferation of cardiac fibroblasts had significant difference between each groups(F=71.84,P=0.000).The proliferation of cardiac fibroblasts with Ang II stimulation was higher than that of cells without Ang II stimulation(P〈0.05).Astragalus membranaous inhibited Ang II-induced cardiac fibroblasts proliferation dose dependently(P〈0.05).The TGF-β1 production had significant difference between each groups(F=786.81,P=0.000).The TGF-β1 production in Ang II/astragalus membranaous groups was lower than that in Ang II group(P〈0.05).The TGF-β1 production in Ang II group was the highest,and had significant difference as compared to other groups(P〈0.05).Astragalus membranaous inhibited Ang II-induced TGF-β1 production dose dependently(P〈0.05).Conclusions Ang II can stimulate the proliferation of cardiac fibroblasts,and promote the TGF-β1 production.Astragalus membranaous can inhibit the proliferation of Ang II-induced cardiac fibroblasts,and reduce the TGF-β1 production of cardiac fibroblasts.
出处
《临床儿科杂志》
CAS
CSCD
北大核心
2015年第3期284-286,共3页
Journal of Clinical Pediatrics
基金
湖南省教育厅科研基金资助项目(No.13C522)
湖南省中医药科研计划项目(No.2014105)