Abstract

To explore the effect of electroacupuncture(EA) preconditioning on cerebral infarct volume and the contents of TNF-α, IL-10 in serum of rats with cerebral ischemia-reperfusion injury. Thirty-six rats were randomly divided into a sham operation group, a model group and an EA preconditioning group, 12 rats in each group, which were further divided into 12 h and 24 h after reperfusion subgroups, 6 rats in each one. EA was used before model establishment for 2 weeks in the EA preconditioning group. The model of cerebral ischemia-reperfusion injury in rats was established with modified Longa suture method. 12 h and 24 h after reperfusion, the degree of neurological deficit was assessed by the modified behavioral scoring scale; the cerebral infarct volume was measured by TTC method and the contents of TNF-α, IL-10 in serum were detected by ELISA method. Compared with the model group, the neurological severity scores in the EA preconditioning group significantly reduced 12 h and 24 h after reperfusion (both P<0.05), the cerebral infarct volume in the EA preconditioning group significantly reduced 12 h and 24 h after reperfusion (both P<0.05). Compared with the sham operation group, the serum TNF-α, IL-10 contents in the model group increased 12 h and 24 h after reperfusion (both P<0.05). Compared with the model group, the serum TNF-α content reduced, while the serum IL-10 content increased in the EA preconditioning group 12 h after reperfusion (both P<0.05). Compared with the model group, the serum TNF-α, IL-10 contents reduced in the EA preconditioning group 24 h after reperfusion (both P<0.05). EA preconditioning can improve neurological deficit, reduce cerebral infarct volume after cerebral ischemia-reperfusion injury in rats. The mechanism may be related to the regulation of EA on the dynamic balance between pro-inflammatory cytokine TNF-α and anti-inflammatory cytokine IL-10 in peripheral blood of cerebral ischemia-reperfusion injury in acute phase, thus alleviate acute cerebral ischemia-reperfusion inflammatory response.

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