Roles of PI3K/Akt and JAK/STAT signal transduction pathways in reduction of myocardial ischemia/reperfusion injury by postconditioning with α7nAChR agonist in rats
10.3760/cma.j.issn.0254-1416.2012.07.032
- VernacularTitle:PI3K/Akt和JAK/STAT信号转导通路在α7nAChR激动剂后处理减轻大鼠心肌缺血再灌注损伤中的作用
- Author:
Jun XIONG
;
Fushan XUE
;
Qiang WANG
;
Yujing YUAN
;
Xu LIAO
;
Yi CHENG
;
Ruiping LI
;
Jianhua LIU
;
Tianzuo LI
- Publication Type:Journal Article
- Keywords:
1-Phosphatidylinositol 3-kinase;
Protein-serine-threonine kinases;
Receptors,nicotinic;
Myocardial reperfusion injury
- From:
Chinese Journal of Anesthesiology
2012;32(7):886-889
- CountryChina
- Language:Chinese
-
Abstract:
Objective To evaluate the roles of PI3K/Akt and JAK/STAT signal transduction pathways in reduction of myocardial ischemia/reperfusion (I/R) injury by postconditioning with α subunit-containing nicotinic acetylcholine receptor (α7nAChR) agonist in rats.Methods Sixty Sprague-Dawley rats,weighing 290-320 g,were randomly divided into 4 groups (n =15 each):I/R group,ischemic preconditioning group (IPC group),ischemic postconditioning group (IPOC group) and postconditioning with specific α7nAChR agonist PNU282987 group ( PNU group ).Myocardial I/R was produced by 30 min occlusion of left anterior descending coronary artery followed by 180 min reperfusion in the 4 groups.The animals were subjected to 3 cycles of 5 min myocardial ischemia and 5 min reperfusion before 30 min myocardial ischemia in IPC group.The animals underwent 3 cycles of 10 s myocardial ischemia at 5 s intervals before 180 min reperfusion in group IPOC.PNU282987 2.4 mg/kg was injected intraperitoneally immediately before the reperfusion.At 60 min of reperfusion,5 rats in each group were sacrificed and the hearts were removed to determine the expression of Akt and STAT3 mRNA,phosphorylated Akt (p-Akt) and phosphorylated STAT3 (p-STAT3) in myocardial tissues.The left 10 rats in each group were sacrificed at 180 min of reperfusion and the hearts were removed to measure the infarct size.Results Compared with I/R group,the expression of STAT3 mRNA and p-Akt was significantly up-regulated in IPC group,and the expression of p-Akt and p-STAT3 was significantly up-regulated in IPOC group ( P ＜ 0.05).The infarct size was significantly reduced in IPC,IPOC and PNU groups compared with I/R group ( P ＜ 0.05 ).Conclusion The mechanism by which α7nAChR agonist postconditioning reduces myocardial I/R injury is not related to PI3K/Akt and JAK/STAT signal transduction pathways in rats.
