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  

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

作　　者：刘艺 徐卫娟[2] 柯丽[2] 李云桥[2] 彭雯[2] 

机构地区：[1]亚洲心脏病医院心外科,湖北武汉430022 [2]华中科技大学同济医学院附属协和医院老年医学科,湖北武汉430022

出　　处：《基础医学与临床》2013年第7期864-867,共4页Basic and Clinical Medicine

基　　金：湖北省自然科学基金(2011CDB382)

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200～250 g,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。Objective To investigate the role of Creatine phosphate in myocardial ischemia-reperfusion（I/R） inju- ry of rat heart. Methods Twenty-four male SD rats weighing 200 - 250 g, were randomly divided into a Sham group ; a I/R group and a phosphocreative （CP） group. CP group were taken the intravenous administration of 4 mg/kg creatine phosphate sodium before the reperfusion. TUNEL method was used to detect apoptosis of cardio- myocytes. The formation of autophagosomes was observed by electron microscopy. Expression of LC3-Ⅱ was meas- ured by the Western blot. Results Comparing with sham group, I/R aggravated injury of mitochondria, and in- creased autophagic vacuoles（AVs） （P 〈 0. 01 ） and apoptosis of cardiomyocytes （P 〈 0.01 ）. However, CP group alleviated injury of mitochondria and reduced 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 was less increased than I/R-injured rats（ P 〈 0.05 ）. Conclusions Creatine phosphate inhibitsapoptosis and excessive autophagy to diminish the cell death induced by the myocardial I/R injury.

关 键 词：自噬 缺血再灌注损伤 磷酸肌酸 凋亡 

分 类 号：R654.2[医药卫生—外科学]