RESUMO
OBJECTIVE: To observe the effect of electroacupuncture (EA) of "Dingzhongxian" (MS 5) and "Dingpangxian" (MS 8) on the expression of cerebral protein kinase C (PKC) isozymes in local cerebral ischemia reperfusion injury (CI/RI) rats so as to explore its underlying mechanism in protecting ischemic brain tissue. METHODS: Seventy-two Wistar rats were randomized into normal control (n = 8), CI/RI model (model, n = 32), and EA (n = 32) groups. The later two groups were further divided into 4, 12, 24 and 72 h subgroups, respectively, with 8 rats in each. CI/RI model was established by occlusion of the middle cerebral artery under anesthesia and reperfusion for 4, 12, 24 and 72 h, respectively. EA (1 mA, 2 Hz/15 Hz) was applied to "Dingzhongxian" (MS5) and "Dingpangxian" (MS8) for 10 min every time, and once again every 12 h after modeling. The expression of PKCgamma and PKCdelta in the ischemic cortex tissue was detected using immunohistochemistry. TdT-mediated dUTP Nick-End Labeling was used to detect neuronal apoptosis of the local ischemic cerebral cortex. RESULTS: In comparison with the normal group, the expression levels of cerebral PKCgamma and PKCdelta proteins as well as the number of the apoptotic neurons at time-points of 4, 12, 24 and 72 h after modeling were increased apparently in the model group (P < 0.01); while compared with the model group, cerebral PKCgamma and PKCdelta protein expressions and the apoptotic neuronal number were decreased considerably in the EA group (P < 0.01, P < 0.05). No significant differences were found among the 4 time-points in the expression levels of PKCgamma and PKCdelta and apoptotic neuronal number in the model group and EA group (P > 0.05). CONCLUSION: EA intervention can effectively down-regulate expressions of cerebral PKCgamma, PKCdelta proteins and apoptotic neuronal number in cerebral ischemia rats, which may contribute to its effect in protecting the ischemic cerebral tissue.
