Protective effects of trimetazidine on mitochondral in myocardial ischemia reperfusion rats
- VernacularTitle:曲美他嗪对大鼠缺血再灌注心肌线粒体的保护作用
- Author:
Yanfang ZHAO
;
Yongwen QIN
;
Xuemin WANG
;
Mingyong MIAO
- Publication Type:Journal Article
- Keywords:
Trimetazidine;
Ischemia-reperfusion injury;
Mitochondrial;
Oxygen-derived free radicals
- From:
Journal of Medical Postgraduates
2005;0(S1):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To study the protective effects of trimetazidine (TMZ) on mitochondrial in myocardial ischemia reperfusion rats and its mechanism. Methods: Fifty SD rats were randomly divided into four groups; the pseudooperation group, the saline group and two TMZ treated groups(5 mg/kg and 10 mg/kg). In the pseudooperation group, the coronary artery was not ligated, but the chest was opened. Other groups were subjected to myocardial ischemia reperfusion injury. The serum level of mal onaldehyole ( MDA ) , superoxide dismutase ( SOD ) , glutathione ( GSH ) , glutathione peroxidase (GSH-PX) and the accumulation of Ca2+ in myocardial mitochondrial were detected at the time of 30 min ischemia and 40 min reperfusion. The myocyte ultrastnicture was also observed by electron microscope in the four groups. Results: Compared with the pseudooperation group, the MDA and total Ca2+ were significantly higher and the SOD, GSH, and GSH-PX were significantly lower in saline group and treatment groups. Compared with the saline group, the MDA and total Ca2+ was significantly lower and the SOD, GSH, and GSH-PX were significantly higher in the treatment groups. Conclusion: TMZ could significantly reduce lipid peroxidation in myocardial mitochondrial induced by ischemia and ische-mia-reperfusion. The mechanism may be that TMZ could increase the content of GSH and the acvitity of SOD and GSH-PX, and enhance its antioxidant production. TMZ could protect the cardiac cells by reducing calcium overload in myocardial mitochondrial.
