Electro-acupuncture At Points Of Zusanli And Quchi Exerts Neuroprotective Effect Through The Modulation Of PI3I/Akt Signalling Pathway

We evaluated the neuroprotective effect of electro-acupuncture (EA) on cerebral ischemia-reperfusion (IR) injury and deeply investigate the relationship between this neuroprotective effect and PI3k Akt pathway. Rats underwent focal cerebral IR injured by suture method and received the in vivo therapeutic efficacy of EA at points of Zusanli(ST36) and Quchi(LIII) at24h.48h.72h after the operation. We found that significant (P<0.05) differences were observed in terms of neurological deficit scores between and among EA and IC groups at48h and72h after the cerebral IR injury rats. In addition, treatment with EA significantly (P<0.05) improved cerebral infarction. Furthermore. EA profoundly activated P13K/Akt signaling resulted in the inhibition of cerebral cell apoptosis in the ischemic penumbra. Simultaneously EA increased the expression of PI3K. p-Akt. p-Bad and Bcl-2at the protein level and the expression of Bcl-2at the mRNA level. On the contrary. EA inhibited the Bax and cleaved Caspase-3-positive expression. The selective PI3K inhibitor LY294002compromised EA-induced neuroprotective effects, and reduced the elevation of p-Akt. p-Bad and Bcl-2levels. Our datas lead us to suggest that the PI3K Akt pathway play a critical role in mediating the neuroprotective effects of EA treatment at points of Zusanli and Quchi after ischemic stroke.