基础医学与临床 ›› 2011, Vol. 31 ›› Issue (11): 1247-1250.

• 研究论文 • 上一篇    下一篇

姜黄素预处理对急性心肌缺血大鼠心肌细胞凋亡相关因子表达的影响

高建芝1,李东亮2,王永玲3,张金盈3   

  1. 1. 河南省 新乡医学院 基础医学院
    2. 新乡医学院生理教研室
    3.
  • 收稿日期:2010-08-23 修回日期:2010-12-23 出版日期:2011-11-05 发布日期:2011-11-02
  • 通讯作者: 高建芝 E-mail:gaoteng.bao@163.com
  • 基金资助:
    省科技发展项目

Effect of Curcumin Preconditioning on Expression of Myocardial Apoptosis-related Factor in Acute Myocardial Ischemia in rats

  • Received:2010-08-23 Revised:2010-12-23 Online:2011-11-05 Published:2011-11-02
  • Contact: Gao Jian-Zhi E-mail:gaoteng.bao@163.com

摘要: 【摘要】 目的 探讨姜黄素预处理对急性心肌缺血大鼠心肌细胞凋亡相关因子表达的影响。方法 30只SD雄性大鼠随机分为姜黄素预处理组、心肌缺血2h组及假手术组,采用冠状动脉结扎的方法建立大鼠心肌缺血模型。用TUNEL法观察各组大鼠的心肌细胞凋亡情况;采用RT-PCR检测各组大鼠心肌细胞bcl-2及caspase-3 mRNA的表达水平,并探讨它们之间的关系。结果 与心肌缺血组相比,姜黄素预处理组bcl-2 mRNA的表达水平明显升高,心肌细胞凋亡数与bcl-2 mRNA表达量之间成明显的负相关(r=-0.93, P<0.05);姜黄素预处理组caspase-3 mRNA的表达水平降低,心肌细胞凋亡数与caspase-3 mRNA表达量值之间成明显的正相关(r=0.89, P<0.05)。结论 姜黄素对心肌缺血大鼠模型心肌梗死有明显保护作用,其作用机制可能与调节心肌细胞凋亡相关因子作用有关。

关键词: 心肌缺血, 姜黄素, 心肌, 凋亡相关因子

Abstract: 【Abstract】0bjective to investigate the effect of curcumin preconditioning on expression of myocardial apoptosis-related factor in acute myocardial ischemia (AMI) in rats. Methods Thirty SD male rats were randomly divided into acute myocardial ischemia injury rats group, sham-operation group and curcumin-treated AMI group. Detected myocardial apoptosis with the terminal deoxynucleotidyl transferase mediated dUTP nick end labeling (TUNEL) technique of all rats.Then infered their apoptosis index.We detected myocardial apoptosis-related factor with RT-PCR technique of all rats and investigated their relations.Results Compared with acute myocardial ischemia injury rats group,their mRNA levels of bcl-2 in curcumin-treated AMI group increased markedly, the myocardial apoptosis index related positively with their mRNA levels of bcl-2; their mRNA levels of caspase-3 in curcumin-treated AMI group decreased signaficantly, the myocardial apoptosis index related negtively with their mRNA levels of caspase-3. Conclusions Curcumin have obviously protective effects on myocardial infarction in the myocar- dial ischemia rats.The mechanism possible related with regulation apoptosis-related factor.

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