RESUMEN
Objective To evaluate 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 .Methods A total of 60 Male adult SD rats were randomly divided into five groups:sham control group(SC ,n=12) ,ischemia control group ,(IC group , n=12) electro‐acupuncture group(EA group ,n= 12) ,EA + DMSO group(DMSO group ,n= 12) and EA + LY294002 group (LY2940002 group ,n=12) .Rats in the IC group、EA group、DMSO group and LY2940002 group underwent 2 h of middle cerebral artery occlusion(MCAO) ,followed by 72 h of reperfusion .DMSO or LY294002 was injected into the lateral ventricle at 30 min be‐fore the ischemia .Rats of the IC group ,EA group ,DMSO group and LY2940002 group received electro‐acupuncture at 24 h after the operation and continued until animals were sacrificed at 72 h after the operation ,and the stimulation parameters were set as fol‐lows :disperse wave ,30 min of each time ,once a day .Neurological deficit scores were assessed at 24 h ,48 h and 72 h after the IR in‐jury .The infarct volume was determined at 72 h after the IR injury using TTC staining .Apoptotic cells in the cerebral cortex were quantified under confocal fluorescence microscope using TUNEL staining .The expression of PI3K ,Akt ,p‐Akt ,Bad and p‐Bad at the protein level was assessed by Western blotting .Results Significant differences were observed in terms of neurological deficit scores between and among the EA group ,DMSO group and other groups at 48 h and 72 h after the cerebral IR injury(P<0 .05) .At 72 h after the cerebral IR injury ,the infarct volume of the IC group and LY294002 group was significantly larger than those of the EA group and DMSO group(P<0 .05) .Compared with the IC group and LY294002 group ,EA treatment greatly reduced the number of apoptotic nerve cells(P<0 .01) .The expression of PI3K ,p‐Akt and p‐Bad at the protein level in the EA group and DMSO group were higher than those of the IC group and LY294002 group(P<0 .05) .Conclusion EA treatment at points of Zusanli(ST36) and Quchi(LI11) exerted the neuroprotective effect on the cerebral IR injury through the modulation of PI3K/Akt pathway .