Effect of electroacupuncture preconditioning on neurological deficit and expression of cerebral Cx43 protein in rats with acute cerebral infarction / 针刺研究

ABSTRACT

OBJECTIVE: To observe the effect of electroacupuncture (EA) on expression of cerebral Cx43 protein in acute cerebral infarction (ACI) rats so as to explore its mechanisms underlying improvement of ACI. METHODS: Sixty male SD rats were randomly divided into sham operation, model and EA preconditioning groups (n＝20 in each group). Fourteen days before modeling, the rats in the EA preconditioning group accepted EA stimulation (3 Hz/15 Hz, 1 mA) at Dingzhongxian (MS5) and Dingpangxian (MS8) for 30 min, once daily, 6 times a week for 2 weeks. The ACI model was established by occlusion of the middle cerebral artery for 120 min, followed by reperfusion. Twenty-four hours after modeling, the neurological function was evaluated according to the Zea-Longa's score criteria. The triphenyltetrazolium chloride (TTC) staining method was used to detect the cerebral infarct volume. The expression levels of Cx43, phosphorylated (p)-Cx43 and PKC proteins in the right cerebral cortical infarction region were detected by Western blot. RESULTS: The neurological function scores and the infarct volume were significantly higher in the model group than those in the sham operation group (P<0.05), and obviously lower in the EA preconditioning group than in the model group (P<0.05). The expression level of cerebral Cx43 protein was significantly increased (P<0.05), and those of p-Cx43 and PKC proteins were notably decreased in the model group relevant to the sham operation group (P<0.05). In the EA preconditioning group, the expression level of Cx43 was significantly decreased and those of p-Cx43 and PKC proteins were significantly increased than those in the model group (P<0.05). CONCLUSION: EA pretreatment can relieve neurological damage and reduce cerebral infarction volume in ACI rats, which may be related to its function in promoting Cx43 protein phosphorylation via up-regulating PKC expression in the ischemic cerebral region.