基础医学与临床 ›› 2013, Vol. 33 ›› Issue (7): 864-867.

• 研究论文 • 上一篇    下一篇

磷酸肌酸减少大鼠缺血再灌注心肌细胞凋亡及自噬泡的数量

刘艺1,徐卫娟2,柯丽3,李云桥3,彭雯3   

  1. 1. 武汉亚洲心脏病医院心外科病房
    2. 华中科技大学同济医学院附属协和医院老年科
    3. 武汉协和医院
  • 收稿日期:2012-11-09 修回日期:2013-01-27 出版日期:2013-07-05 发布日期:2013-06-26
  • 通讯作者: 彭雯 E-mail:pengwen365@sina.com
  • 基金资助:
    Beclin 1与Bcl-2/xl在冬眠心肌细胞中的新关系

Creatine phosphate decreases the apoptosis and autophagy in myocardial ischemia/reperfusion rat heart

  • Received:2012-11-09 Revised:2013-01-27 Online:2013-07-05 Published:2013-06-26
  • Contact: Wen Peng E-mail:pengwen365@sina.com

摘要: 目的 研究磷酸肌酸减少大鼠缺血再灌注心肌细胞凋亡及自噬的能力。方法 雄性SD大鼠24只,体质量200g~250g,随机均分为假手术(Sham)组、缺血/再灌注(Ischemia-Reperfusion,I/R)组和磷酸肌酸钠(Phosphocreatine,CP)干预组。其中CP组按4 mg/kg磷酸肌酸钠剂量于再灌注前经右股静脉注射。用TUNEL法检测心肌细胞凋亡;电子显微镜观察心肌细胞自噬泡的发生和线粒体的形态学改变;Western blot检测微管相关蛋白1轻链 3-II (LC3-II)蛋白的表达。结果 I/R组与Sham组相比,线粒体超微结构损伤加重,自噬泡数量增多(P<0.01),心肌细胞凋亡率明显增加(P<0.01);CP干预组可减轻I/R组线粒体超微结构损伤,自噬泡数量减少(P<0.05),降低心肌细胞凋亡率(P<0.05);LC3-II作为评价自噬强度的指标,I/R组与Sham组相比,LC3-II蛋白的表达明显上调(P<0.01).;而CP与I/R组相比,该蛋白表达明显下调(P<0.05)。结论 磷酸肌酸通过减少大鼠缺血再灌注心肌细胞凋亡及自噬泡的数量,从而减轻心肌缺血再灌注损伤。

关键词: 自噬, 缺血再灌注损伤, 磷酸肌酸, 凋亡

Abstract: Objective To investigate the role of Creatine phosphate in myocardial ischemia-reperfusion (I/R) injury of rat heart in vivo. Methods 24 male SD rats weighing 200g~250g, were randomly divided into a Sham group; a I/R group and a Creatine phosphate(CP)group. CP group used the intravenous administration of 4 mg/kg Creatine Phosphate Sodium before the reperfusion. TUNEL method was used to detect apoptosis of cardiomyocytes. The formation of autophagosomes was observed by transmission electron microscopy. Expression of LC3-II was measured by the Western blotting. Results Comparing with Sham group, I/R aggravates injury of mitochondria, and increase autophagic vacuoles (AVs) (P<0.01) and apoptosis of cardiomyocytes (P<0.01). However, CP group alleviates injury of mitochondria and reduce autophagic vacuoles (P<0.05) and apoptosis of cardiomyocytes (P<0.05) comparing to I/R group. LC3-II formation, an autophagy marker, was down-regulated in the CP group (P<0.01), which less increased than I/R-injured rats (P<0.05). Conclusion These results suggest that Creatine phosphate inhibits apoptosis and excessive autophagy to diminish the cell death induced by the myocardial I/R injury.

Key words: autophagy, Ischemia-reperfusion injury, Creatine phosphate, apoptosis