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目的 观察小剂量线粒体毒素 3 硝基丙酸 (3 nitroppropionicacid ,3 NPA)预处理对大鼠局灶性脑缺血后促红细胞生成素 (erythropoietin ,Epo)蛋白和mRNA表达的影响 ,揭示 3 NPA预处理诱导脑缺血耐受的机制。 方法 大鼠腹腔注射 3 NPA 3d后制作大鼠局灶性缺血再灌注模型 ,采用TTC染色、免疫组织化学方法、逆转录聚合酶链式反应技术 ,观察 3 NPA预处理对缺血 2h再灌注 2 4h脑梗死体积和Epo蛋白及mRNA表达的影响。 结果 脑缺血再灌注后Epo蛋白表达广泛 ,主要分布于缺血侧基底节区、海马和部分大脑皮质。 3 NPA预处理使脑梗死体积减小 ,Epo蛋白和mRNA的表达增多 ,与对照组比较有显著性差异。结论 小剂量 3 NPA预处理可以诱导脑缺血耐受 ,脑源性Epo表达增强可能是其形成的机制之一。
Objective To investigate the effect of 3 NPA pretreatment on protein and mRNA expression of erythropoietin (Epo) after focal cerebral ischemia in rats, and to investigate the effect of 3 NPA preconditioning Mechanisms to deal with induction of cerebral ischemic tolerance. Methods Rats were injected intraperitoneally with 3-NPA for 3 days to make a rat model of focal ischemia-reperfusion. TTC staining, immunohistochemistry and RT-PCR were used to observe the effects of 3-NPA preconditioning on ischemia reperfusion Effect of 24 hours cerebral infarction volume and Epo protein and mRNA expression. Results Epo protein was widely expressed after cerebral ischemia-reperfusion in ischemic basal ganglia, hippocampus and part of the cerebral cortex. 3 NPA preconditioning reduced the volume of cerebral infarction and the expression of Epo protein and mRNA increased significantly compared with the control group. Conclusion Low-dose 3-NPA preconditioning can induce cerebral ischemic tolerance, and the enhancement of brain-derived Epo expression may be one of its mechanisms.