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[Effect of electroacupuncture on cerebral PKC isozyme expression levels in cerebral ischemia-reperfusion rats].

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.