Involvement of ERK 1/2 activation in electroacupuncture pretreatment via cannabinoid CB1 receptor in rats
Involvement of ERK 1/2 activation in electroacupuncture pretreatment via cannabinoid CB1 receptor in rats
复制标题
ERK 1/2 激活参与大鼠大麻素 CB1 受体电针预处理
DOI：
10.1016/j.brainres.2010.07.034
复制
发表时间：
2010-11-11
期刊：
影响因子：
2.9
通讯作者：
Chen, Shaoyang
中科院分区：
文献类型：
--
作者：
Du, Juan;Wang, Qiang;Chen, Shaoyang
我们之前的研究表明，电针预处理（EA）通过大麻素受体1型受体（CB1R）对短暂性脑缺血有保护作用。在本研究中，我们研究了细胞外信号调节激酶1/2 （ERK1/2）通路是否通过CB1R参与EA预处理诱导的缺血耐受。最后一次EA预处理结束后24 h，阻断大鼠大脑中动脉致局灶性脑缺血120 min。再灌注后24 h评估神经学评分和梗死体积。在CB1R拮抗剂AM251存在或不存在的情况下，也研究了p-ERK1/2在脑中的表达。在再灌注后24小时，EA预处理可减少梗死面积并改善神经转归，U0126可消除这种有益作用。AM251阻断CB1R可逆转EA预处理诱导的p-ERK1/2表达上调。我们的研究结果提示ERK1/2通路可能通过大麻素CB1受体参与EA预处理诱导的大鼠脑缺血耐受。(C) 2010爱思唯尔公司版权所有。
Our previous study demonstrated that pretreatment with electroacupuncture (EA) elicited protective effects against transient cerebral ischemia through cannabinoid receptor type 1 receptor (CB1R). In the present study, we investigated whether or not the extracellular signal regulated-kinase 1/2 (ERK1/2) pathway was involved in the ischemic tolerance induced by EA pretreatment through CB1R. At 24 h after the end of the last EA pretreatment, focal cerebral ischemia was induced by middle cerebral artery occlusion for 120 min in rats. The neurological scores and infarct volumes were evaluated at 24 h after reperfusion. The expression of p-ERK1/2 in the brains was also investigated in the presence or absence of CB1R antagonist AM251. EA pretreatment reduced infarct volumes and improved neurological outcome at 24 h after reperfusion, and the beneficial effects were abolished by U0126. The blockade of CB1R by AM251 reversed the up-regulation of p-ERK1/2 expression induced by EA pretreatment. Our findings suggest that the ERK1/2 pathway might be involved in EA pretreatment-induced cerebral ischemic tolerance via cannabinoid CB1 receptor in rats. (C) 2010 Elsevier Inc. All rights reserved.