Ginkgo biloba extract reducing myocardium cells apoptosis by regulating apoptotic related proteins expression in myocardium tissues

被引:29
作者
Qiao, Zeng Yong [1 ,2 ]
Huang, Jian Hua [1 ]
Ma, Jiang Wei [1 ]
Xu, Ya Wei [2 ]
Xie, Jun [3 ]
Liu, Hua Jin [1 ]
Xiong, San Jun [1 ]
Ge, Guang Hao [1 ]
机构
[1] Shanghai 6th Peoples Hosp, Fengxian Branch, Dept Cardiol, Shanghai 201400, Peoples R China
[2] Tongji Univ, Peoples Hosp 10, Dept Cardiol, Shanghai 200092, Peoples R China
[3] Nanjing Univ, Sch Med, Dept Cardiol, Nanjing 210008, Jiangsu, Peoples R China
基金
中国国家自然科学基金;
关键词
Apoptosis; Bax; Cyt-c; Myocardium ischemia reperfusion; caspase-3; Western blot; BCL-2; FAMILY; CYTOCHROME-C; ACTIVATION; DEATH; STRESS; MITOCHONDRIA; ISCHEMIA; INFARCT;
D O I
10.1007/s11033-013-2868-9
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The Bax, cyt-c and caspase-3 proteins play an important role in regulating the myocardial apoptosis. Although very little is known about the specific signal pathways modulated by Ginkgo biloba extract (GBE), it seems advisable to suppose that GBE-induced antiapoptotic effect might be attributed to the regulation of the expression of these proteins. Our aim was to investigate whether GBE could attenuate ischemia/reperfusion-induced apoptosis in cardiac myocytes and its potential mechanisms. In the myocardium ischemia reperfusion (IR) rat model, treatment of GBE (400 mg/kg) significantly decreased the cardiomyocyte cell apoptosis and myocardium infarction. Immunohistochemical analysis showed that GBE significantly inhibited I/R-induced increase of myocardial Bax, caspase-3, and cyt-c proteins expression. Western blot analysis confirmed results of immunohistochemical analysis. It is most likely that multiple pathways are involved in IR-induced apoptosis in rat myocardium cells. Therefore, these results demonstrate that GBE exhibits significant protective effect against myocardial I/R injury in rat heart, which is related to down-regulate Bax, cyt-c and caspase-3. Bcl-2 overexpression might prevent IR-induced apoptosis by inhibiting cytochrome c release from the mitochondria and block activation of caspase-3.
引用
收藏
页码:347 / 353
页数:7
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