| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 4326263 | Brain Research | 2010 | 7 Pages |
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.
Research Highlights►Electroacupuncture (EA) pretreatment up-regulates phospho-ERK1/2. ►EA pretreatment induces the ischemic tolerance in brain. ►A specific inhibitor of ERK abolishes neuroprotection of EA pretreatment. ►A CB1 receptor antagonist inhibits up-regulation of p-ERK1/2 by EA pretreatment. ►ERK1/2 pathway involves in EA pretreatment via cannabinoid CB1 receptor.
