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背景:肌苷参与机体多方面的代谢过程,对缺血性脑损伤具有一定的保护作用,但其机制还没有彻底阐明。目的:研究肌苷对大鼠脑缺血再灌注后血管内皮生长因子(vascularen-dothelialgrowthfactor,VEGF)表达的影响,探讨肌苷的神经保护作用机制。设计:随机对照的实验研究。地点和材料:本实验在青岛大学医学院脑血管病研究所和山东省脑血管病防治重点实验室完成。成年健康雌性SD大鼠68只,体质量230～270g,清洁级,由中国科学院上海实验动物中心提供。干预措施:成年健康雌性SD大鼠68只,应用线栓法建立SD大鼠大脑中动脉阻塞(MCAO)再灌注模型,随机分为治疗组32只和对照组32只,每组再随机分为缺血1.5h再灌流2,6,12,24h,2,3,7,14d组(n=4),另外4只作假手术组。应用免疫组织化学方法检测脑缺血再灌流后脑组织VEGF的表达。结果:假手术组脑组织未见VEGF阳性表达。对照组在皮层区和纹状体区VEGF在脑缺血再灌注2h开始表达,12h达高峰,持续24h,随即迅速降低。VEGF阳性细胞主要位于Ⅱ,Ⅲ,Ⅳ层神经元和血管内皮细胞,尤其神经细胞核周细胞浆和树突染色最深。肌苷治疗组VEGF表达于缺血再灌注2h～2d较对照组显著增高,经统计学处理,差异有非常显著性意义(t=3.78～22.62,P<0.01)。结论:肌苷可上调脑缺血再灌注后VEGF的表达,可能是其缺?
BACKGROUND: Inosine participates in many aspects of the body’s metabolic processes and has some protective effects on ischemic brain injury. However, its mechanism has not been fully elucidated. Objective: To study the effect of inosine on the expression of vascular endothelial growth factor (VEGF) after cerebral ischemia-reperfusion in rats and to explore the neuroprotective mechanism of inosine. Design: Randomized controlled experimental study. Location and Materials: This experiment was performed at the Institute of Cerebrovascular Diseases, Medical College of Qingdao University and Key Laboratory of Prevention and Treatment of Cerebrovascular Diseases in Shandong Province. 68 adult healthy female SD rats, body weight 230 ~ 270g, clean level, provided by the Shanghai Laboratory Animal Center, Chinese Academy of Sciences. Interventions: Sixty-eight adult female Sprague-Dawley rats were randomly divided into treatment group (n = 32) and control group (n = 32). Each group was then randomly divided into After ischemia 1.5h and reperfusion 2, 6, 12, 24h, 2, 3, 7 and 14d groups (n = 4), the other 4 were sham operation groups. Immunohistochemistry was used to detect the expression of VEGF in brain tissue after cerebral ischemia and reperfusion. Results: There was no positive expression of VEGF in sham operation group. The control group in the cortex and striatum VEGF expression began 2h after cerebral ischemia-reperfusion, peaked at 12h, lasting 24h, then rapidly decreased. VEGF positive cells mainly located in layer II, III and IV neurons and vascular endothelial cells, especially in the nuclei of peripheral nerve cells and dendritic staining the most. In the group of inosine treatment, the expression of VEGF was significantly increased from 2 h to 2 d after ischemia-reperfusion, and the difference was statistically significant (t = 3.78 ~ 22.62, P <0.01). Conclusion: Inosine can up-regulate the expression of VEGF after cerebral ischemia-reperfusion, which may be the lack of it.