Abstract: OBJECTIVE  To observe the improvement degree of nerve function and the effect of electroacupuncture on autophagy related proteins LC3-Ⅱ and Beclin1 expression in rats with cerebral ischemia-reperfusion injury.METHODS  According to the random number table method, 72 male SD rats were randomly divided into control group, model group and electroacupuncture group, with 24 rats in each group. A modified rat model of acute focal cerebral ischemia reperfusion was established by referring to Longa line bolt method, and reperfusion was performed 1 h after ischemia. The degrees of cerebral neurological damage of the three groups of rats were evaluated by using the improved Zea Longa grade 8 neurological impairment score. Electroacupuncture intervention was performed at 5 min and 16 h after successful modeling. Materials were harvested 24 h after reperfusion. The cerebral infarction volumes of rats in each group were observed by TTC staining. The histopathological changes of rat brain were observed by HE staining. The expression of LC3-Ⅱ and Beclin1 protein in the right striatum of rats brain tissue were tested by Western blot assay, and the expression of Beclin1 mRNA was detected by qPCR.RESULTS  No behavioral change was observed in the control group, and the neurological function score of the model group was significantly higher than that of the control group (P < 0.05). Compared with the model group, the score of nerve function defect in the electroacupuncture group was significantly lower than that in the model group (P < 0.05). The volume of cerebral infarction in the electroacupuncture group was significantly lower than that in the model group (P < 0.05). Compared with the model group, the expression of LC3-Ⅱ and Beclin1 protein in the electroacupuncture group significantly increased (P < 0.05), and the expression of Beclin1 mRNA significantly increased (P < 0.05).CONCLUSION  Electroacupuncture therapy may regulate the occurrence of autophagy by promoting the expression of autophagy-related proteins LC3-Ⅱ and Beclin1, reduce the volume of cerebellar infarction, improve the neurological function defect, and achieve the protective effect on rats with cerebral ischemia-reperfusion injury.