Department of Anesthesiology, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China.
Brain Res. 2010 Nov 11;1360:1-7. doi: 10.1016/j.brainres.2010.07.034. Epub 2010 Jul 21.
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 24h after the end of the last EA pretreatment, focal cerebral ischemia was induced by middle cerebral artery occlusion for 120min in rats. The neurological scores and infarct volumes were evaluated at 24h 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 24h 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.
我们之前的研究表明，电针（EA）预处理通过大麻素受体 1 型受体（CB1R）引发对短暂性脑缺血的保护作用。在本研究中，我们通过 CB1R 研究细胞外信号调节激酶 1/2（ERK1/2）通路是否参与 EA 预处理诱导的缺血耐受。在最后一次 EA 预处理结束后 24 小时，通过大脑中动脉闭塞诱导大鼠 120 分钟的局灶性脑缺血。再灌注后 24 小时评估神经功能评分和梗死体积。还研究了存在或不存在 CB1R 拮抗剂 AM251 时大脑中 p-ERK1/2 的表达。EA 预处理可减少再灌注后 24 小时的梗死体积并改善神经功能，而 U0126 可消除这些益处。AM251 阻断 CB1R 可逆转 EA 预处理诱导的 p-ERK1/2 表达上调。我们的研究结果表明，ERK1/2 通路可能通过大鼠中的大麻素 CB1 受体参与 EA 预处理诱导的脑缺血耐受。
