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目的初步探讨外源性给予尿酸对脑缺血的保护作用及其机制。方法大脑中动脉线栓法制作大鼠局灶性脑缺血再灌注模型。动物随机分为假手术组、缺血模型组、溶媒对照组、尿酸(62.5 mg·kg-1.d-1,93.75 mg·kg-1.d-1)治疗组、阿司匹林阳性对照组。手术后断头取脑,行神经行为学评分和TTC染色法判断神经元损伤程度。取缺血侧皮质组织,分光光度法测定丙二醛(MDA)、一氧化氮(NO)、黄嘌呤氧化酶(XO)含量和超氧化物歧化酶(SOD)、谷胱甘肽过氧物酶(GSH-Px)活力的变化;用ELISA方法检测神经元型一氧化氮合酶(nNOS)含量变化。结果尿酸可以改善脑缺血再灌注大鼠神经行为学评分(P<0.05)、降低脑缺血再灌注大鼠皮质损伤(P<0.05),从而起到神经保护作用。尿酸可减少缺血侧皮质组织MDA,XO含量(P<0.05)、抑制SOD,GSH-PX活力升高(P<0.05),并降低nNOS含量。结论尿酸可通过其抗氧化应激效应以及降低nNOS和XO含量对大鼠局灶性脑缺血发挥保护作用。
Objective To investigate the protective effect of exogenous uric acid on cerebral ischemia and its mechanism. Methods The focal cerebral ischemia-reperfusion model was established by middle cerebral artery occlusion in rats. The animals were randomly divided into sham operation group, ischemia model group, vehicle control group, uric acid (62.5 mg · kg -1 · d -1,93.75 mg · kg -1 · d -1) and aspirin positive control group. After surgery, the brain was decapitated, and neurobehavioral score and TTC staining were used to determine the degree of neuronal injury. The ischemic cortex tissues were taken out and the contents of malondialdehyde (MDA), nitric oxide (NO), xanthine oxidase (XO) and superoxide dismutase (SOD), glutathione peroxidase Enzyme (GSH-Px) activity changes; using ELISA method to detect changes in neuronal nitric oxide synthase (nNOS) content. Results Uric acid can improve neurological behavioral score (P <0.05), reduce cerebral cortex injury (P <0.05), and thus play a neuroprotective role in cerebral ischemia-reperfusion rats. Uric acid decreased the content of MDA and XO in ischemic cortex tissue (P <0.05), inhibited the activity of SOD and GSH-PX (P <0.05) and decreased the content of nNOS. Conclusion Uric acid exerts a protective effect on focal cerebral ischemia in rats through its anti-oxidative stress effects and the reduction of nNOS and XO levels.