CAJ | 학술논문

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。
목적：탐토IMD1-53대혈관긴장소Ⅱ（ AngⅡ）유도적대서심기성섬유세포효원대사적조절작용。방법배양신생SD대서심기성섬유세포，장기분성대조조、AngⅡ＋불동농도IMD1-53조。 Westem blot법검측심기성섬유세포Ⅰ화Ⅲ형효원단백표체。 SYBR GreenⅠ형광실시정량PCR검측IMD1-53수체양수체（ CRLR）화전화생장인자-β（ TGF-β） mRNA표체。결과 IMD1-53정제량의뢰성억제AngⅡ유도적심기성섬유세포합성Ⅰ화Ⅲ형효원단백（P＜0.01，P＜0.05）。 IMD1-53정제량의뢰억제성섬유세포TGF-β표체（P＜0.05）。결론 IMD1-53억제AngⅡ유도적심기성섬유세포효원적합성，하조TGF-β표체，가능여IMD1-53항심기섬유화작용유관。
Objective To investigate collagen metabolism modulation of Intermedin 1-53 ( IMD1-53 ) on angiotensin Ⅱ( AngⅡ)-induced rat cardiac fibroblasts .Methods SD neonatal rat cardiac fibroblasts were cultured and divided them into control group, AngⅡ +different concentrations IMD1-53 groups.ⅠandⅢcollagen expression in cardiac fibroblasts were measured by Westem blot , IMD1-53 receptor-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 ob-vious with the increase of IMD 1-53 ( P<0.01 ,P<0.05 ) .Similar phenomenon was recorded in TGF-βexpression in cardiac fibroblasts ( P<0.05 ) .Conclusions IMD1-53 inhibited collagen synthetic in cardiac fibrosis induced by AngⅡ, down-regulated TGF-βexpression.These may relate to IMD1-53 anti myocardial fibrosis.