电针预处理对脑缺血再灌注大鼠大脑皮质一氧化氮合酶及胶质纤维酸性蛋白表达的影响

Effects of Electroacupuncture Preconditioning on Expression of Nitric Oxide Synthase and Glial Fibrillary Acidic Protein in Cortex of Focal Cerebral Ischemia-reperfusion Rats

目的:观察电针预处理对脑缺血再灌注大鼠大脑皮质神经元型一氧化氮合酶(nNOS)、诱导型一氧化氮合酶(iNOS)及胶质纤维酸性蛋白(GFAP)表达的影响,探讨其可能的保护机制。方法:将SD大鼠随机分为假手术组、模型组和电针预处理组,每组8只。采用大脑中动脉栓塞法制备脑缺血再灌注模型。电针预处理组在造模前取"百会"和"大椎"穴给予电针刺激,1次/d,连续7d。造模后24h进行神经功能评分,尼氏染色观察大脑皮质神经细胞形态及存活数,免疫组织化学法检测大脑皮质nNOS、iNOS及GFAP的表达。结果:与假手术组比较,模型组大鼠的神经功能评分明显增高,大脑皮质神经细胞存活数明显减少(P<0.01),nNOS、iNOS及GFAP的表达明显增高(P<0.01);与模型组比较,电针预处理组能明显改善脑缺血再灌注后大鼠的神经功能症状(P<0.01),增加大脑皮质神经细胞的存活数(P<0.01),降低nNOS、iNOS的表达(P<0.01),促进GFAP的表达(P<0.01)。结论:电针预处理对脑缺血再灌注大鼠脑损伤有保护作用,其机制可能与下调nNOS和iNOS、上调GFAP的表达,诱导脑缺血耐受有关。

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 rain, 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 neurotogica/ 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, andup-regulating the expression of GFAP.