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

Abstract

Objective To investigate the role of phosphatidylinositol 3-kinase （PI3K）/protein-serine-thre- onine kinases （Akt） signal pathway in ulinastatin posteonditioning-induced attenuation of apoptosis in myocardial cells in patients undergoing cardiac valve replacement with eardiopulmonary bypass （CPB）. Methods Forty NY- HA class and ASA physical status 11 or m 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- l 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 af- ter aortic unclamping for determination of the expression of Akt, phosphorylated Akt （p-Akt）, cytochrome e, 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 e, 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. Key words: 1-Phosphatidylinositol 3-kinase ; Protein-serine-threonine kinases ; Trypsin inhibitors ; Apoptosis; Cardiopulmonary bypass; Heart valve prosthesis implantation; Postconditioning