Intermedin_(1-53)抑制血管紧张素Ⅱ诱导的大鼠心肌成纤维细胞合成胶原

Intermedin_(1-53) inhibits collagen synthesis induced by angiotensinⅡ in cadiac fibroblasts of rats

目的探讨IMD1-53对血管紧张素Ⅱ(AngⅡ)诱导的大鼠心肌成纤维细胞胶原代谢的调节作用。方法培养新生SD大鼠心肌成纤维细胞,将其分成对照组、AngⅡ+不同浓度IMD1-53组。Westem blot法检测心肌成纤维细胞Ⅰ和Ⅲ型胶原蛋白表达。SYBR GreenⅠ荧光实时定量PCR检测IMD1-53受体样受体(CRLR)和转化生长因子-β(TGF-β)mRNA表达。结果 IMD1-53呈剂量依赖性抑制AngⅡ诱导的心肌成纤维细胞合成Ⅰ和Ⅲ型胶原蛋白(P<0.01,P<0.05)。IMD1-53呈剂量依赖抑制成纤维细胞TGF-β表达(P<0.05)。结论 IMD1-53抑制AngⅡ诱导的心肌成纤维细胞胶原的合成,下调TGF-β表达,可能与IMD1-53抗心肌纤维化作用有关。

Objective To investigate collagen metabolism modulation of Intermedin1-53（ IMD1-53） on angiotensin Ⅱ（ Ang Ⅱ）-induced rat cardiac fibroblasts. Methods SD neonatal rat cardiac fibroblasts were cultured and divided them into control group,AngⅡ ＋ different concentrations IMD1-53 groups. Ⅰ and Ⅲ collagen expression in cardiac fibroblasts were measured by Westem blot, IMD1-53receptor-like receptor（ calcitonin receptor-like receptor,CRLR） and transforming growth factor-β（ TGF-β） mRNA expression were exammed by real-time PCR. Results IMD1-53 significantly inhibited AngⅡ-induced collagen synthesis in cardiac fibroblasts,and this effect was more obvious with the increase of IMD1-53（ P 〈0. 01,P〈 0. 05）. Similar phenomenon was recorded in TGF-β expression in cardiac fibroblasts（ P〈 0. 05）. Conclusions IMD1-53 inhibited collagen synthetic in cardiac fibrosis induced by AngⅡ,down-regulated TGF-β expression. These may relate to IMD1-53 anti myocardial fibrosis.