基础医学与临床 ›› 2015, Vol. 35 ›› Issue (2): 187-190.

• 研究论文 • 上一篇    下一篇

Intermedin1-53抑制血管紧张素Ⅱ诱导的大鼠心肌成纤维细胞合成胶原

孔祥权1,睢燕2,蒋静涵2,许守明2,章辉2   

  1. 1. 皖南医学院第一附属医院(弋矶山医院)
    2. 皖南医学院 第一附属医院
  • 收稿日期:2014-07-03 修回日期:2014-10-22 出版日期:2015-02-05 发布日期:2015-01-23
  • 通讯作者: 孔祥权 E-mail:kongdylan@126.com
  • 基金资助:
    安徽省高校省级科学研究项目;皖南医学院重点科研培育项目

Intermedin1-53 inhibits collagen synthesis induced by angiotensinⅡin cadiac fibroblasts of rats

  • Received:2014-07-03 Revised:2014-10-22 Online:2015-02-05 Published:2015-01-23
  • Contact: Xiang-Quan KONG E-mail:kongdylan@126.com

摘要: 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。

关键词: Intermedin1-53, 心肌成纤维细胞, 血管紧张素Ⅱ, 转化生长因子-β

Abstract: Objective To investigate collagen metabolism modulation of Intermedin1-53 (IMD1-53) on angiotensin Ⅱ (Ang Ⅱ)-induced rat cardiac fibroblasts. Metheds Cultured SD neonatal rat cardiac fibroblasts, and divided them into control group, AngⅡ + different concentrations IMD1-53 groups.Ⅰand Ⅲ collagen 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 by SYBR Green Ⅰ real-time PCR. Results IMD1-53 significantly inhibited AngII-induced collagen synthesis in cardiac fibroblasts, and this effect was more obvious with the increasment of IMD1-53( P < 0.01,P < 0.05). Similar phenomenon took place on TGF-β expression in cardiac fibroblasts( P < 0.05). Conclusion IMD1-53 inhibited collagen synthetic in cardiac fibrosis induced by AngⅡ, downed TGF-β expression. These might relate to IMD1-53 anti myocardial fibrosis.

Key words: Intermedin1-53, cardiac fibroblast, angiotensin Ⅱ, transforming growth factor-β

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