Effect of aminoguanidine on cell apoptosis induced by acute myocardial ischemia in rats
10.3760/cma.j.issn.0254-1416.2014.11.030
- VernacularTitle:氨基胍对大鼠急性心肌缺血时细胞凋亡的影响
- Author:
Meng ZHANG
;
Xinyan ZHANG
;
Fang LIU
;
Qinzeng ZHANG
;
Lijun XIE
;
Hong JIANG
;
Jianxin ZHANG
- Publication Type:Journal Article
- Keywords:
Guanidines;
Myocardical ischemia;
Apopotosis
- From:
Chinese Journal of Anesthesiology
2014;34(11):1393-1395
- CountryChina
- Language:Chinese
-
Abstract:
Objective To evaluate the effect of aminoguanidine on cell apoptosis induced by acute myocardial ischemia in rats.Methods Thirty adult male Sprague-Dawley rats,weighing 250-290 g,were randomly divided into 3 groups (n =10 each):sham operation group (group S),myocardial ischemia group (group Ⅰ),and aminoguanidine group (group AG).The model of acute myocardial ischemia was established by ligating the left anterior descending branch of the coronary artery of rats anesthetized with chloral hydrate.Aminoguanidine 100 mg/kg was intraperitoneally administrated at 6 h of ischemia in AG group,while the equal volume of normal saline was given instead of aminoguanidine in group Ⅰ.The chest was opened at 3 h after aminoguanidine administration and hearts were quickly removed for detection of apoptosis in cardiomyocytes (by TUNEL) and expression of Bcl-2 and Bax in cardiomyocytes (by immuno-histochemistry),and for microscopic examination with light microscope.Apoptotic rate was calculated.Results Compared with group S,the apoptotic rate was significantly increased,the expression of Bax was up-regulated,and the expression of Bcl-2 was downregulated and the ratio of Bcl-2/Bax was decreased in group Ⅰ.Compared with group Ⅰ,the apoptotic rate was significantly decreased,the expression of Bax was down-regulated,and the expression of Bcl-2 was up-regulated,and the ratio of Bcl-2/Bax was increased in group AG.The pathological changes of myocardial cells were significantly attenuated in AG group as compared with group Ⅰ.Conclusion Amionguanidine can inhibit apoptosis in cardiomyocytes and is helpful in mitigating injury induced by acute myocardial ischemia in rats.
