Role of N-myc downstream regulated genes 2 in attenuation of focal cerebral ischemic-reperfusin injury by sevoflurane preconditioning in rats
10.3760/cma.j.issn.0254-1416.2011.09.023
- VernacularTitle:N-myc下游调节基因2在七氟醚预处理减轻大鼠局灶性脑缺血再灌注损伤中的作用
- Author:
Xin LI
;
Peng LUO
;
Feng WANG
;
Shiquan WANG
;
Yan LI
;
Qianzi YANG
;
Xuying LI
;
Qiang WANG
;
Lize XIONG
- Publication Type:Journal Article
- Keywords:
Tumor suppressor proteins;
Anesthetics,inhalation;
Ischemic preconditioning;
Reperfusion injury;
Brain
- From:
Chinese Journal of Anesthesiology
2011;31(9):1110-1113
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the role of N-myc downstream regulated genes 2 (NDRG2) in attenuation of focal cerebral ischemic-reperfusin injury by sevoflurane preconditioning in rats.Methods Forty-eight healthy male SD rats weighing 280-320 g were randomly divided into 3 groups ( n =16 each):sham operation group (group S),ischemia-reperfusion injury group (group I/R) and sevoflurane preconditioning group (group Sev).Focal cerebral ischemia-reperfusion injury was induced by right middle cerebral artery occlusion (MCAO)for 120 min followed by 24 h reperfusion.In group Sev,2.0％ sevoflurane was inhaled 1 h once a day for 5 consecutive days at 24 h before MCAO.The neurologic function was evaluated at 24 h of reperfusion and than the rats were sacrificed,and the brain was removed for determination of infarct volume percentage,NDRG2 and activated Caspase-3 expression in ischemic penumbra by Western Blot and NDRG2 expression and location by immunohistochemistry.Results The infarct volume percentage,NDRG2 and activated Caspase-3 expression were higher,and neurologic function score was lower in groups I/R and Sev then in group S( P ＜ 0.05).The infarct volume percentage,NDRG2 and activated Caspase-3 expression were lower,and neurologic function score was higher in group Sev then in group I/R ( P ＜ 0.05).The intranuclear NDRG2 positive staining was decreased in group Sev than in group I/R.Conclusion Sevoflurane preconditioning can reduce focal cerebral ischemia-reperfusion injury by inhibiting the expression and activity of NDRG2 and apoptosis in rats.
