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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。
OBJECTIVE: To observe the effect of astragaloside IV on the synthesis of type I collagen in Ang II-induced cardiac fibroblasts (CFB) and to explore its mechanism of action against myocardial fibrosis. Methods: The primary CFB was extracted by differential adherence method. Collagen type I synthesis was detected by ELISA. Semi-quantitative RT-PCR was used to detect the expression of collagen I mRNA. RESULTS: Ang II 10-7 mol/L promoted the expression of type I collagen mRNA and myocardial fibroblasts secreted type I collagen. Compared with the blank control group, there was a significant difference; Losartan 10-6 mol/L could reduce type I collagen caused by AngII. The mRNA expression and secretion increased, there was a significant difference between the two; astragaloside 100μg/mL decreased the expression of type I collagen mRNA and secretion increased by AngII, but there was no statistical significance, P> 0.05. Conclusion: Ang II can directly promote the secretion of type I collagen by CFB and significantly increase the expression of type I collagen mRNA. Astragaloside has no obvious inhibitory effect on the increase of Ang II-induced type I collagen mRNA expression and secretion. It is suggested that the production of astragaloside IV against myocardial fibrosis may not be achieved by directly inhibiting the increase of Ang II-induced collagen type I synthesis.