Electroacupuncture pretreatment induces delayed tolerance to focal cerebral ischemia through activation of cannabinoid receptor type 2 in rats
马磊1 侯丽宏1 赵昱1 王强1 朱萧玲1 朱正华1 熊利泽1 贾济1 陈绍洋1
第四军医大学西京医院麻醉科
Background and Purpose：It is well known that pretreatment with electroacupuncture (EA) induces rapid (2h after EA) and delayed (24h after EA) tolerance to focal cerebral ischemia. Our previous study documented that EA pretreatment induced rapid ischemic tolerance to focal cerebral ischemia through regulation of endocannabinoid and up-regulation of the cannabinoid receptor type 1 (CB1). The present study aimed at investigating the involvement of the cannabinoid receptor type 2 (CB2) in the neuroprotection conferred by pretreatment with EA in the rat model of focal cerebral ischemia.
Methods：Separately at 2 and 24 hours after the end of the EA pretreatment, focal cerebral ischemia was induced by middle cerebral artery occlusion for 120 min in male Sprague-Dawley rats. Cerebral ischemic injury was evaluated by neurobehavioral scores and infarction volume percentages 72 hours after reperfusion in the presence or absence of AM251, a selective CB1 receptor antagonist, and AM630, a selective CB2 receptor antagonist. In another experiment, the expression of CB2 receptor in the striatum of ischemic hemisphere of rat brains was detected.
Results：Pretreatment with EA reduces infarction volume percentage, improved neurobehavioral score at 72 hours after reperfusion. AM251 and AM630 could respectively reverse the rapid and delayed ischemic tolerance induced by EA pretreatment. Pretreatment with EA up-regulates the CB2 receptor expression in the striatum of rat brains at 24h after the end of EA stimuli.
Conclusion：These findings suggest that the delayed neuroprotective effect of EA pretreatment against focal cerebral ischemia is through the up-regulation of CB2 receptor in rats, which enriches the mechanism of cerebral protection induced by EA pretreatment.
Methods：Separately at 2 and 24 hours after the end of the EA pretreatment, focal cerebral ischemia was induced by middle cerebral artery occlusion for 120 min in male Sprague-Dawley rats. Cerebral ischemic injury was evaluated by neurobehavioral scores and infarction volume percentages 72 hours after reperfusion in the presence or absence of AM251, a selective CB1 receptor antagonist, and AM630, a selective CB2 receptor antagonist. In another experiment, the expression of CB2 receptor in the striatum of ischemic hemisphere of rat brains was detected.
Results：Pretreatment with EA reduces infarction volume percentage, improved neurobehavioral score at 72 hours after reperfusion. AM251 and AM630 could respectively reverse the rapid and delayed ischemic tolerance induced by EA pretreatment. Pretreatment with EA up-regulates the CB2 receptor expression in the striatum of rat brains at 24h after the end of EA stimuli.
Conclusion：These findings suggest that the delayed neuroprotective effect of EA pretreatment against focal cerebral ischemia is through the up-regulation of CB2 receptor in rats, which enriches the mechanism of cerebral protection induced by EA pretreatment.
