[Effects of electroacupuncture preconditioning on expression of nitric oxide synthase and glial fibrillary acidic protein in cortex of focal cerebral ischemia-reperfusion rats].

OBJECTIVE: To observe the effect of electroacupuncture (EA) preconditioning on the expression of neuronal nitric oxide synthase (nNOS), inducible nitric synthase (iNOS) and glial fibrilliary acidic protein (GFAP) in the cortex of focal cerebral ischemia-reperfusion (CI/R) rats so as to explore its underlying mechanism in the protection of ischemic cerebral tissue. METHODS: Twenty-four Sprague-Dawley rats were randomized into sham operation (sham), model, and EA preconditioning groups (n = 8 in each group). The CI/R model was induced by intraluminal middle cerebral artery occlusion .(MCAO) with a nylon monofilament suture. Before modeling, EA (2 Hz/15 Hz, 3 V) was applied to "Baihui"(GV 20) and "Dazhui"(GV 14) for 30 min, once daily for 7 consecutive days. The neurologic impairment score was assessed by using Longa standards and the survival number of neurons in the local ischemic cerebral cortex was determined after Nissl staining, and the expression of nNOS, iNOS and GFAP in the cerebral cortex was detected using immunohistochemistry. RESULTS: Compared with the sham operation group, the neurological deficit score of the rats in the model group was significantly increased (P < 0.01), and the number of survival neurons of the ischemic cortex was obviously decreased (P < 0.01), and the expression levels of nNOS, iNOS and GFAP were significantly increased in the model group (P < 0.01). In the EA preconditioning group , the neurological deficit score, the expression levels of nNOS and iNOS were significantly down-regulated (P < 0.01), while the number of the survival neurons and GFAP expression level in the ischemic cerebral cortex were obviously higher in the EA preconditioning group in compared with the model group (P < 0.01). CONCLUSION: EA preconditioning can protect the ischemic cerebral cortex tissue from injury in CI/R rats, which may be related to its effects in down-regulating the expression of nNOS and iNOS, and up-regulating the expression of GFAP.