Role of PI3K/Akt signal pathway in ulinastatin postconditioning-induced attenuation of apoptosis in myocardial cells in patients undergoing cardiac valve replacement with cardiopulmonary bypass
10.3760/cma.j.issn.0254-1416.2013.06.001
- VernacularTitle:PI3K/Akt信号转导通路在乌司他丁后处理减轻CPB下心脏瓣膜置换术患者心肌细胞凋亡中的作用
- Author:
Yanbin WANG
;
Xiaolei WANG
;
Weixin CHEN
;
Yujia ZHAI
;
Yijian CHENG
;
Jianan YANG
- Publication Type:Journal Article
- Keywords:
1-Phosphatidylinositol 3-kinase;
Protein-serine-threonine kinases;
Trypsin inhibitors;
Apoptosis;
Cardiopulmonary bypass;
Heart valve prosthesis implantation;
Postconditioning
- From:
Chinese Journal of Anesthesiology
2013;33(6):653-656
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the role of phosphatidylinositol 3-kinase (PI3K)/protein-serine-threonine kinases (Akt) signal pathway in ulinastatin postconditioning-induced attenuation of apoptosis in myocardial cells in patients undergoing cardiac valve replacement with cardiopulmonary bypass (CPB).Methods Forty NYHA class and ASA physical status Ⅱ or Ⅲ patients of both sexes,aged 21-59 yr,scheduled for cardiac valve replacement with CPB,were randomly divided into 2 groups (n =20 each):normal saline control group (group C) and ulinastatin postconditioning group (group U).In group U,ulinastatin 10 000 U/kg was perfused via the aortic root at 4000-5000 U· kg-1 · min-1 starting from 5 min before aortic unclamping.In group C,the equal volume of normal saline was given instead of ulinastatin.Myocardial specimens were taken from the right auricle at 45 min after aortic unclamping for determination of the expression of Akt,phosphorylated Akt (p-Akt),cytochrome c,caspase-9,Bcl-2 and Bax,and cell apoptosis.Bcl-2/Bax ratio and apoptotic index were calculated.Results The expression of p-Akt and Bcl-2 and Bcl-2/Bax ratio were significantly higher,and the expression of cytochrome c,caspase-9 and Bax and apoptotic index were lower in group U than in group C (P < 0.05).Conclusion Ulinastatin postconditioning attenuates apoptosis in myocardial cells in patients undergoing cardiac valve replacement with CPB through activating PI3K/Akt signal pathway.