Role of reperfusion injury salvage kinase signaling pathway in reduction of myocardial ischemia-reperfusion injury by sevoflurane postconditioning in rats
10.3760/cma.j.issn.0254-1416.2017.06.030
- VernacularTitle:RISK信号通路在七氟醚后处理减轻大鼠心肌缺血再灌注损伤中的作用
- Author:
Huatong LI
;
Nengxin FANG
;
Dong CHEN
;
Lihuan LI
- Keywords:
Anesthetics,inhalation;
MAP kinase signaling system;
Myocardial reperfusion injury;
Ischemic postconditioning
- From:
Chinese Journal of Anesthesiology
2017;37(6):754-757
- CountryChina
- Language:Chinese
-
Abstract:
Objective To evaluate the role of reperfusion injury salvage kinase signaling pathway in reduction of myocardial ischemia-reperfusion (I/R) injury by sevoflurane postconditioning in rats.Methods Seventy SPF healthy adult male Sprague-Dawley rats,weighing 300-350 g,were divided into 7 groups (n =10 each) using a random number table:sham operation group (group S),group I/R,sevoflurane postconditioning group (group SP),phosphatidylinositol 3-kinase inhibitor LY294002 group (group LY),sevoflurane postconditioning plus LY294002 group (group SPLY),mitogen-activated protein kinase kinase 1/2 inhibitor U0126 group (group U) and sevoflurane postconditioning plus U0126 group (group SPU).Myocardial I/R was induced by occlusion of the left anterior descending branch of the coronary artery for 30 min followed by 120 min of reperfusion.In group SP,1.8％ sevoflurane was inhaled for 5 min starting from the beginning of reperfusion.In LY and U groups,LY294002 0.3 mg/kg and U0126 0.5 mg/kg were intravenously injected,respectively,at 10 min before reperfusion.In SPLY and SPU groups,LY294002 0.3 mg/kg and U0126 0.5 mg/kg were intravenously injected,respectively,at 10 min before reperfusion,and 1.8％ sevoflurane was inhaled for 5 min starting from the beginning of reperfusion.At 15 min of reperfusion,myocardial specimens were obtained from the left ventricular area at risk for determination of the phosphorylation of protein kinase B (Akt) and extra-cellular signal-regulated kinase 1/2 (ERK1/2) (by Western blot) and NAD+ content in myocardial tissues (by fluorescence spectrophotometry).At the end of reperfusion,blood samples were collected from the jugular vein for measurement of serum cardiac troponin Ⅰ (cTnI) concentrations (by photoelectric colorimetry),and myocardial specimens were obtained from the left ventricular area at risk for determination of myocardial infarct size (IS).Resuits Compared with group S,the IS and serum cTnI concentrations were significantly increased,the NAD+ content was decreased (P＜0.05),and no significant change was found in the phosphorylation of Akt or ERK1/2 in group I/R (P＞0.05).Compared with group I/R,the IS and serum cTnI concentrations were significantly decreased,and the NAD+ content and phosphorylation of Akt and ERK1/2 were increased in group SP (P＜0.05),and no significant change was found in the parameters mentioned above in LY,SPLY,U and SPU groups (P＞0.05).Compared with group SP,the IS and serum cTnI concentrations were significantly increased,and the NAD+ content was decreased in SPLY and SPU groups,the phosphorylation of Akt was significantly decreased in group SPLY,and the phosphorylation of ERK1/2 was significantly decreased in group SPU (P＜0.05).Conclusion The mechanism by which sevoflurane postconditioning reduces myocardial I/R injury may be related to activation of reperfusion injury salvage kinase signaling pathway in rats.
