Role of autophagosomes clearance in delayed cardioprotection in rats with ischemia-reperfusion injury by sevoflurane preconditioning in vivo
10.3760/cma.j.issn.1671-0282.2017.01.013
- VernacularTitle:自噬小体清除在七氟烷预处理延迟性心肌保护中的作用
- Author:
Shigang QIAO
;
Bo SUN
;
Haihua SHAN
;
An WANG
;
Jia QIU
;
Chen WANG
- Keywords:
Anesthetic,inhalation;
Myocardial reperfusion injury;
Autophagy;
Apoptosis;
Lysosome
- From:
Chinese Journal of Emergency Medicine
2017;26(1):65-70
- CountryChina
- Language:Chinese
-
Abstract:
Objective To evaluate role of autophagosomes clearance in delayed cardioprotection by sevoflurane preconditioning in rats with ischemia-reperfusion injury in vivo.Methods Forty-five adult male Sprague-Dawley rats,weighing 270-350 g,were randomly (random number) divided into 3 groups:sham operation group (sham group),ischemia-reperfusion group (CON group),sevoflurane preconditioning group (SWOP group).Myocardial ischemia was induced by 30 min occlusion of left anterior descending branch (LAD) of coronary artery followed by reperfusion for 2 h,and myocardial infarct size was stained by triphenyltetrazolium chloride.Cardiomyocyte apoptosis was evaluated by terminal deoxyribonucleotidyl transferase-mediated biotin-16dUTP nick-end labeling.Autophagosomes were detected under transmission electron microscope.Expression of LC3-Ⅱ,cathepsin B,p62 and cleaved caspase-3 were assessed by western blotting.Statistical analysis were performed using one or two way analysis of variance (SPSS 15.0,Chicago,USA) test followed by Dunnet-t or LSD-t test.Results Sevoflurane preconditioning reduced myocardial infarct size and the number of autophagosomes (P =0.027),attenuated cardiomyocyte apoptosis (P =0.042).Sevoflurane preconditioning decreased the level of LC3-Ⅱ (P =0.033),p62 (P =0.041)and cleaved caspase-3 (P =0.037),but increased the level of cathepsin B (P =0.046).Conclusions Delayed cardioprotection by sevoflurane preconditioning increased myocardial clearance of autophagosomes against the delayed ischemia reperfusion injury.
