基础医学与临床 ›› 2010, Vol. 30 ›› Issue (3): 289-292.

• 研究论文 • 上一篇    下一篇

促红细胞生成素减轻大鼠心肌缺血再灌注损伤

郭晋村 黄卫斌 王挹青 谢良地   

  1. 厦门大学附属中山医院心内科 厦门大学附属中山医院心内科 福建省高血压研究所
  • 收稿日期:2009-04-03 修回日期:2009-08-02 出版日期:2010-03-05 发布日期:2011-05-04
  • 通讯作者: 黄卫斌

Erythropoietin reduces myocardial ischemia-reperfusion injury in rats

Jin-cun GUO, Wei-bin HUANG, Yi-qing WANG, Liang-di XIE   

  1. Department of Cardiology, Zhongshan Hospital Xiamen Unviersity Department of Cardiology, Zhongshan Hospital Xiamen Unviersity Fujian Hypertension Research Institute
  • Received:2009-04-03 Revised:2009-08-02 Online:2010-03-05 Published:2011-05-04
  • Contact: Wei-bin HUANG,

摘要: 目的 探讨促红细胞生成素在心肌缺血再灌注损伤中对细胞外基质代谢的调节作用及其机制。方法 构建Langendroff大鼠离体心脏缺血再灌注模型,结合Western blot观测在促红细胞生成素及相应信号传导通路阻滞剂干预下,左室舒张末压(LVDP)、梗死面积、MMPs及CollagenaseI/III表达的变化 结果 促红细胞生成素可改善LVDP(19.8+0.2mmHg vs 35.9+0.2mmHg,IR group vs EPO+IR group,p<0.05),减少梗死面积(35.26%+7.1% vs 62.70%+7.2% EPO+IR group vs IR group,p<0.05)。在缺血再灌注损伤的过程中MMP2及MMP9表达均显著升高,而TIMP-4则显著减低。外源性EPO可逆转MMPs的激活。此外EPO则可促进CollagenIII、I的表达,并且这一保护作用可被MEK-Erk信号通路阻滞剂所阻断。结论EPO通过MEK-Erk信号传导通路促进CollagenI/III的合成、抑制MMPs的激活、抑制细胞外基质降解,在一定程度上减轻大鼠心肌缺血再灌注损伤。

关键词: 促红细胞生成素, 细胞外基质, 缺血再灌注损伤

Abstract: Objective To investigate the influence of erythropoietin in the metabolism of extracellular matrix after myocardial ischemia-reperfusion injury. Method The langendroff reperfusion system was applied to investigate the protect function of EPO on the ischemia-reperfusion condition in rats. The effects of EPO on extracellular matrix were observed by western blot and signal pathway blocker. The LVDP and infarction area were observed at the same time. Results: EPO significantly improved LVDP(19.8+0.2mmHg vs 35.9+0.2mmHg,IR group vs EPO+IR group,p<0.05)and decreased infarction area (35.26%+7.13% vs 62.70%+7.23% IR group vs EPO+IR group,p<0.05). The MMPs expressions were significantly attenuated and Collagenase I/III were significantly enhanced by EPO(MMP2 53.2+2.6vs21.2+2.5; MMP9 57.6+3.1vs 19.2+2.6; IR组vs IR+EPO组, p<0.05 ;CollagenI 43.2+2.2vs11.4+2.3; CollagenIII 55.3+3.2vs 18.1+2.3; IR+EPO组vs IR组, p<0.05 ). This function can be inhibited by Mek-Erk inhibitor. Conclusion: EPO play a role in the metabolism of extracellular matrix by Mek-Erk signal pathway, which can protect the heart tissue from ischemia-reperfusion injury.

Key words: erythropoietin, extracellular matrix, ischemia-reperfusion injury