Dl-3-n-butylphthalide inhibits myocardial infarction in acute myocardial ischemia
- VernacularTitle:丁苯酞抑制大鼠急性心肌缺血导致的心肌损伤
- Author:
Ming SUN
;
Jun CHU
;
Hongjun ZHU
- Publication Type:Journal Article
- Keywords:
Dl-3-n-butylphthalide;
coronary artery ligation;
mitochondria infaction;
apoptosis index;
myocardial infarction
- From:
Acta Universitatis Medicinalis Anhui
2014;(9):1206-1209
- CountryChina
- Language:Chinese
-
Abstract:
Objective To observe the effects of Dl-3-n-butylphthalide ( NBP) on the mitochondria infarction, size of myocardial infarction and myocardial apoptosis after acute myocardial ischemia in rats. Methods 92 male SD rats were divided into sham operation group (8 rats) , model group (21 rats) , and low-dose NBP group (21 rats) , medium-dose NBP group (21 rats) , high-dose NBP group (21 rats) . The model and NBP groups were made into MI model by ligation of the left anterior descending ( LAD) coronary artery, but not in sham-operated group. Model group and NBP group were taken heart specimens after coronary artery ligation. Cardiomyocyte apoptosis was ana-lyzed by TUNEL in each group. Size of MI was analyzed by TTC staining in sham-operated group, model group and high-dose NBP group. Electron perspective microscopy was applicated in observing mitochondria infarction in model group and high-dose NBP group after myocardial infarction. The expressions of Bcl-2 protein and Bax protein were detected by Western blot. Results Compared with model group, butylphthalide significantly increased expression of Bcl-2 protein ( P <0.05 ) and the ratio of Bcl-2/Bax ( P <0.05 ) , inhibited mitochondria infarction ( P <0.05 ) , reduced myocardial infarct size ( P<0.01 ) and cardiomyocyte apoptosis ( P<0.05 ) . Conclusion Bu-tylphthalide significantly inhibits myocardial infarction by increasing expression of Bcl-2 protein and the ratio of Bcl-2/Bax and decreasing mitochondria infarction, reducing myocardial infarct size and cardiomyocyte apoptosis in rats during the acute myocardial ischemia process.
