基础医学与临床 ›› 2014, Vol. 34 ›› Issue (3): 295-300.

• 研究论文 • 上一篇    下一篇

促红细胞生成素抑制AngⅡ诱导的大鼠心肌细胞肥大及其可能的信号通路

赵金红,王伟,张新金,李建美   

  1. 云南省第二人民医院
  • 收稿日期:2013-02-27 修回日期:2013-06-25 出版日期:2014-03-05 发布日期:2014-02-27
  • 通讯作者: 张新金 E-mail:zxjgry2004@sina.com
  • 基金资助:
    自发性高血压大鼠心、脑、肾和肠系膜微动脉缝隙连接特性的比较研究》国家自然科学基金(国家自然科学基金);云南省自然科学基金

Erythropoietin attenuates Cardiomyocytes hypertrophy induced by Ang Ⅱ and its possible signal pathway in rats

  • Received:2013-02-27 Revised:2013-06-25 Online:2014-03-05 Published:2014-02-27

摘要: 目的 观察促红细胞生成素(EPO)对新生大鼠心肌细胞肥大中信号通路蛋白表达的影响。方法 用血管紧张素Ⅱ(AngⅡ, 10-6mol/L)诱导心肌细胞肥大,分别以EPO(2×104U/L)或/和P38丝裂原活化蛋白激酶(MAPK)抑制剂SB203580(15μmol/L)进行干预,检测心肌细胞表面积、蛋白合成、胚胎基因ANF及β-MHC表达,Real-Time-Q-PCR检测转化生长因子β(TGF-β)1及P38MAPK mRNA表达;Western blot法检测TGF-β1、TGF-β激活性激酶1(TAK1)、phospho-TAK1、P38MAPK和phospho-P38MAPK蛋白的表达。结果 EPO能有效抑制AngⅡ诱导的心肌细胞肥大(p<0.05),抑制TGF-β1、TAK1、phospho-TAK1、P38MAPK和phospho-P38MAPK表达(p<0.05);SB203580能增强EPO抑制心肌细胞肥大的作用。结论 EPO能减轻AngⅡ诱导的心肌细胞肥大,其可能与TGF-β1-TAK1-P38 MAPK信号通路有关。

关键词: 促红细胞生成素,心肌细胞肥大,TGF-β1,TAK1,p38MAPK

Abstract: Objective To observe the effects of erythropoietin ( EPO) on angiotensinⅡ ( AngⅡ ) induced neonatal rat cardiomyocyte hypertrophy and its signal protein expression. Methods Cardiomyocytes were isolated from new-born Sprague-Dawley rats and were used to establish the model of hypertrophy by AngII in vitro.The cells was treated with EPO or/and P38MAPK inhibitor SB203580. The cell surface area, [3H]-leucine incorporation ,mRNA expression of atrial natriuretic factor(ANF) and β-myosin heavy chain(β-MHC) of cardiomyocytes were employed to detect cardiomyocyte hypertrophy. The mRNA levels of TGF-β1 and P38MAPK was analyzed by real-time quantitative PCR. The protein expression of TGF-β1、TAK1、P38MAPK and phosphorylation of TAK1 and P38MAPK were analyzed by Western blot. Results EPO attenuated hypertrophy of cardiomyocytes. EPO significantly suppressed TGF-β1、TAK1、P38MAPK、phosphrylation of TAK1 and P38MAPK expression. SB203580 represses cardiac hypertrophy. Conclusions EPO attenuates cardiomyocytes hypertrophy induced by Ang II,and it might be associated with TGF β1-TAK1-P38MAPK signaling pathway.

Key words: erythropoietin,cardiocyte hypertrophy,TGF-β1,TAK1,p38MAPK

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