Effects of isoflurane postconditioning on cerebral ischemia-reperfusion injury in rats
10.3760/cma.j.issn.0254-1416.2013.08.023
- VernacularTitle:异氟醚后处理对大鼠脑缺血再灌注损伤的影响
- Author:
Fangxiang ZHANG
;
Qian ZHAO
;
Jingchao ZHANG
;
Weijing ZHANG
;
Bing QIU
- Publication Type:Journal Article
- Keywords:
Isoflurane;
Ischemic preconditioning;
Brain;
Reperfusion injury;
Postconditioning
- From:
Chinese Journal of Anesthesiology
2013;33(8):993-996
- CountryChina
- Language:Chinese
-
Abstract:
Objective To evaluate the effects of isoflurane postconditioning on cerebral ischemia-reperfusion (I/R) injury in rats.Methods Thirty-two male Sprague-Dawley rats,weighing 280-320 g,were randomly divided into 4 groups (n=8 each):group sham operation (group S),group I/R,group isoflurane preconditioning (group Ⅰ-pre),and group isoflurane postconditioning (group Ⅰ-post).Global cerebral I/R was induced by 4-vessel occlusion method described by Pulsinelli.1.5％ isoflurane was inhaled for 2h before ischemia in group Ⅰ-pre.1.5％ isoflurane was inhaled for 30 min immediately after onset of reperfusion in group Ⅰ-post.Neurological function was assessed and scored at 24h of reperfusion.The rats were sacrificed at 72h of reperfusion and hippocampi were isolated for determination of neuronal apoptosis (by TUNEL),caspase-3 expression (by immuno-histochemistry),and phosphorylated c-Jun N-terminal kinase (p-JNK) protein expression (by using Western blot) in hippocampal tissues.Apoptotic rate was calculated.Results Compared with S group,the number of grid cross was decreased,twist time was prolonged,hanging time was shortened,apoptotic rate was increased,and the expression of caspase-3 and p-JNK protein was up-regulated in I/R,I-pre and Ⅰ-post groups (P ＜ 0.05).Compared in I/R group,the number of grid cross was increased,twist time was shortened,hanging time was prolonged,apoptotic rate was decreased,and the expression of caspase-3 and p-JNK protein was down-regulated in Ⅰ-pre and Ⅰ-post groups (P ＜ 0.05).Compared with I/R group,the number of grid cross was decreased,hanging time was shortened,apoptotic rate was increased,and the expression of caspase-3 was up-regulated (P ＜ 0.05),and no significant changes in the expression of p-JNK protein were found in Ⅰ-post group (P ＞ 0.05).Conclusion Isoflurane postconditioning can reduce cerebral I/R injury,the efficacy is weaker than that of preconditioning and the mechanism is related to activation of JNK signal transduction pathway and inhibition of neuronal apoptosis in hippocampus of rats.
