【摘要】 目的:通过观察黄芪甲苷对AngⅡ诱导的心肌成纤维细胞(CFB)Ⅰ型胶原合成的影响,探讨其抗心肌纤维化的作用机制。方法:差速贴壁法提取原代CFB,采用ELISA法检测Ⅰ型胶原合成,RT-PCR法半定量检测Ⅰ胶原mRNA表达。结果:AngⅡ10-7mol/L有促进Ⅰ型胶原mRNA表达及心肌成纤维细胞分泌Ⅰ型胶原的作用,与空白对照组比较,有显著性差异;Losartan10-6mol/L可降低AngⅡ引起的Ⅰ型胶原mRNA表达及分泌增加,两者比较有显著性差异;黄芪甲苷100μg/mL有降低AngⅡ引起Ⅰ型胶原mRNA表达及分泌增加的趋势,但无统计学意义,P>0.05。结论:AngⅡ可直接促进CFB分泌Ⅰ型胶原,并能显著增加Ⅰ型胶原mRNA的表达;黄芪甲苷对AngⅡ诱导的Ⅰ型胶原mRNA表达及分泌增加未见明显抑制作用。提示,黄芪甲苷抗心肌纤维化作用的产生可能不是通过直接抑制AngⅡ诱导的Ⅰ型胶原的合成增加来实现的。更多还原

【Abstract】 Objective:To observe Astragalosides on type Ⅰ collagen synthesis of rat cardiac fibroblasts that induced by AngⅡ,expecting to explore the mechanism of action by Astragalosides in myocardial fibrosis.Methods:Isolated and cultured cardiac myofibroblast from neonatal rats were used as experiment model.The secretion of Collagen Ⅰ was measured by ELISA.The expression of mRNA of TypeⅠcollagen was measured by RT-PCR.Results:The secretion of type I collagen,and the expression of mRNA of type Ⅰ collagen increased with AngⅡ were significantly higher than those of control group.The group of AngⅡ+Astragalosides could decreased the secretion and the expression of mRNA of type I collagen.But it was not significantly in statistics.Conclusion:The effect of Astragalosides on the synthesis and expression of mRNA of typeⅠcollagen that increased by AngⅡ is not obviously.This shows that the mechanism of Astragalosides in myocardial fibrosis is not across the passway of direct repression of the increase of type Ⅰ collagen induced by AngII.更多还原