Effects of phosphocreatine on apoptosis following myocardial ischemia-reperfusion in diabetic melllitus rats
10.3760/cma.j.issn.0254-1416.2011.06.028
- VernacularTitle:磷酸肌酸对糖尿病大鼠心肌缺血再灌注时细胞凋亡的影响
- Author:
Jianhua CHANG
;
Guixia JING
;
Xuyun DANG
- Publication Type:Journal Article
- Keywords:
Phosphocreatine;
Diabetes mellitus,experimental;
Myocardial repeffusion injury;
Apoptosis
- From:
Chinese Journal of Anesthesiology
2011;31(6):746-749
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of phosphocreatine on apoptosis following myocardial ischemia-reperfusion (I/R) in diabetic rats. Methods Male SD rats weighing 150-170 g were used in this study.Diabetes mellitus was induced by high fat diet and intraperitoneal streptozotocin. Twenty-seven rats in which diabetes mellitus was successfully induced were randomly divided into 3 groups ( n = 9 each): sham operation group (group S);myocardial I/R group(group I/R )and phosphocreatine group (group PP). Myocardial I/R was induced by 30 min occlusion of left anterior descending branch of coronary artery followed by 2 h reperfusion in I/R and PP groups. In group PP phosphocreatine 1 g/kg was given intraperitoneally 30 min before myocardial I/R. Blood samples were collected at the end of 2 h reperfusion for determination of plasma concentration of calcium troponin T (cTnT). The animals were then sacrificed and iscbemic myocardial specimens were isolated. The expression of Bcl-2, Bax and Caspase-3 in isehemic myocarcdium was determined and Bcl-2/Bax ratio was calculated. Myocardial apoptosis was detected by TUNEL and apoptotic index was calculated. The ultrastructure of cardiomyocytes was examined with electron microscope. Results Myocardial I/R significantly increased plasma cTnT concentration and Bcl-2, Bax and Caspase-3 expression in myocardium and apoptosis index and decreased Bcl-2/Bax ratio. Phosphocreatine significantly attenuated I/R-induced above-mentioned changes and myocardial damage. Conclusion Phosphocreatine can reduce myocardial I/R injury in diabetic mellitus rats by reducing myocardial apoptosis through up-regulation of Bcl-2 expression and down-regulation of Bax and Caspase-3 expression.
