Effect of delayed preconditioning with morphine on ischemic cerebral injury in mice and the role of classical protein kinase C
10.3760/cma.j.issn.0254-1416.2013.04.026
- VernacularTitle:吗啡延迟预处理对小鼠缺血性脑损伤的影响及经典型蛋白激酶C在其中的作用
- Author:
Xiaoyan ZHAO
;
Jiefei LI
;
Song HAN
;
Junfa LI
;
Tianzuo LI
- Publication Type:Journal Article
- Keywords:
Morphine;
Ischemic pretreatment;
Brain ischemia;
Protein kinase C
- From:
Chinese Journal of Anesthesiology
2013;(4):490-492
- CountryChina
- Language:Chinese
-
Abstract:
Objective To evaluate the effect of delayed preconditioning with morphine on ischemic cerebral injury in mice and the role of classical protein kinase C (cPKC).Methods Forty male BALB/C mice,weighing 20-22 g,were randomly divided into 4 groups (n =10 each):sham operation group (group S),ischemic cerebral injury group (group ICI),morphine preconditioning group (group MP) and cPKC inhibitor Go6983 group (group G).Ischemia was induced by middle cerebral artery occlusion (MCAO).In S group,the middle cerebralartery was only exposed but not occluded.In MP group,morphine 10 mg/kg was injected intraperitoneally 24 h before MCAO.In G group,morphine 10 mg/kg was injected intraperitoneally 24 h before MCAO and 5 μl Go6983 (6nmol) was injected into the left lateral cerebral ventricle immediately before MCAO.The neurologic deficit was evaluated and scored according to neurological disability status scale in a blind nanner 6 h after MCAO.The animals were sacrificed and brains were immediately removed for measurement of the brain edema and infarct volume.Apoptotic rate was calculated.Results Compared with S group,the neurologic deficit scores,infarct volume,brain edema and apoptotic rate were significantly increased in ICI,MP and G groups (P ＜ 0.01).Compared with group ICI,the neurologic deficit scores,infarct volume,brain edema and apoptotic rate were significantly decreased in group MP (P ＜ 0.01),and no significant change was found in the parameters mentioned above in group G (P ＞ 0.05).Conclusion Delayed preconditioning with morphine can reduce ischemic cerebral injury in mice and activation of classical cPKC signaling pathway is involved in the mechanism.
