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目的探讨血管紧张素II(Ang II)促进心脏成纤维细胞胶原合成的分子机制,初步分析miR-21在其中发挥的作用。方法使用SD大鼠心脏组织分离培养原代成纤维细胞;分别使用0、0.1、0.2和0.4μmol/L的Ang II刺激细胞36 h,qRT-PCR检测胶原(Col1a1和Col3a1)和miR-21的表达变化;使用miR-21抑制物(miR-21 inhibitor)转染细胞,Ang II刺激后,qRT-PCR检测Col1a1和Col3a1的表达。结果镜下观察和标志物分子检测表明心脏成纤维细胞培养成功。在Ang II刺激下,Col1a1、Col3a1和miR-21均呈剂量依赖性表达增加(P<0.05)。使用miR-21抑制物能显著降低Ang II刺激下Col1a1和Col3a1的表达升高(P<0.05)。结论 Ang II能增加心脏成纤维细胞的胶原合成,其相关机制可能部分通过miR-21相关信号来介导。
Objective To investigate the molecular mechanism of angiotensin II (Ang II) promoting cardiac fibroblast collagen synthesis and to analyze the role of miR-21 in it. Methods Primary fibroblasts were isolated and cultured in SD rat heart tissue. Cells were stimulated with Ang II at 0, 0.1, 0.2 and 0.4 μmol / L for 36 h, respectively. The expression of collagen (Col1a1 and Col3a1) and miR-21 The expression of Col1a1 and Col3a1 was detected by qRT-PCR after Ang II stimulation. Results Microscopic observation and molecular marker tests showed that cardiac fibroblasts were cultured successfully. Under Ang II stimulation, Col1a1, Col3a1 and miR-21 increased in a dose-dependent manner (P <0.05). Using miR-21 inhibitor significantly reduced the expression of Col1a1 and Col3a1 (P <0.05) under Ang II stimulation. Conclusions Ang II can increase the collagen synthesis in cardiac fibroblasts, and its related mechanism may be partly mediated by miR-21 related signals.