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[Effect of electroacupuncture preconditioning on neurological deficit and expression of cerebral Cx43 protein in rats with acute cerebral infarction].

电针 医学 麻醉 脑梗塞 大脑中动脉 梗塞 内科学 刺激 闭塞 免疫印迹 内分泌学 缺血 针灸科 病理 心肌梗塞 生物化学 化学 基因 替代医学
作者
Ting Yin,Haiping Chen,Wen Wang,Wei Zhang,Juan Huang
出处
期刊:Acupuncture Research 卷期号:44 (7): 497-500
标识
DOI:10.13702/j.1000-0607.190067
摘要

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.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.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).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.
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