Effect of sufentanil postconditioning on Ac-H3 expression during myocardial ischemia-reperfusion in rats
10.3760/cma.j.issn.0254-1416.2016.02.032
- VernacularTitle:舒芬太尼后处理对大鼠心肌缺血再灌注时Ac-H3表达的影响
- Author:
Xianya ZHAO
;
Erwei GU
;
Xianfu LU
;
Lei ZHANG
;
Manli CHEN
;
Senlin DONG
- Publication Type:Journal Article
- Keywords:
Sufentanil;
Ischemic postconditioning;
Myocardial reperfusion injury;
Histones;
Acetylation
- From:
Chinese Journal of Anesthesiology
2016;36(2):246-249
- CountryChina
- Language:Chinese
-
Abstract:
Objective To evaluate the effect of sufentanil postconditioning on acetylated histon H3 (Ac-H3) expression during myocardial ischemia-reperfusion (I/R) in rats.Methods Thirty-six adult male Sprague-Dawley rats,weighing 250-300 g,were randomly divided into 3 groups (n =12 each) using a random number table:sham operation group (S group),I/R group,and sufentanil postconditioning group (SP group).Myocardial I/R was induced by 30 min occlusion of the left anterior descending branch of the coronary artery followed by 120 min reperfusion in anesthetized rats.Sufentanil 1 μg/kg was injected through the femoral vein at 5 min before reperfusion in group SP,while the equal volume of normal saline was given in S and I/R groups.The rats were sacrificed at 120 min of reperfusion,and the myocardial specimens were obtained from the anterior wall of the left ventricle for determination of myocardial infarct size and cell apoptosis (by TUNEL),and myocardial specimens were obtained from the apex for detection of Ac-H3 expression (using Western blot).Apoptotic index was calculated.Results Compared with S group,the myocardial infarct size and apoptotic index were significantly increased,and Ac-H3 expression was down-regulated in I/R and SP groups (P＜0.05).Compared with I/R group,the myocardial infarct size and apoptotic index were significantly decreased,and Ac-H3 expression was up-regulated in SP group (P＜ 0.05).Conclusion Sufentanil postconditioning attenuates myocardial I/R injury through up-regulating AcH3 expression and restoring histone acetylation in rats.
