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机构地区:[1]天津市神经病学研究所神经生化研究室
出 处:《中风与神经疾病杂志》1999年第2期67-69,共3页Journal of Apoplexy and Nervous Diseases
基 金:天津市科委资助
摘 要:目的探讨脑缺血后再灌流海马结构选择性易损伤的分子机制。方法采用阻断大鼠两侧颈总动脉结合放血制备前脑缺血再灌流损伤动物模型,应用Northern杂交、原位杂交及免疫组织化学技术,检测了egr-1及bcl-2基因的表达和组织学分布。结果发现易损伤的海马CA1区锥体细胞的egr-1及bcl-2基因表达受抑制,而耐受缺血的海马CA3区锥体细胞则明显表达这两种蛋白,并且这两种基因表达的组织学分布具有惊人的一致性。结论提示EGR-1及BCL-2蛋白参与损伤神经元的修复,对神经元有保护作用;EGR-1蛋白可能参与bcl-2基因表达的调控。Objective To study the molecular mechanism of selective vulnerability of hippocampal formation in transient cerebral ischemia.Methods The model were induced in Wistar rats exposed to transient forebrain ischemia.The expression and distribution of egr 1 and bcl 2 genes in these regions were detected by northern hybridization,in situ hybridization and immunohistochemistry methods.Results It was found that the expression of egr 1 and bcl 2 genes were inhibited in CA 1 region vulnerable to ischemia,while the two genes expressed in high level in CA 3 region resistant to ischemia.The distribution of egr 1 expression conincided with that of bcl 2.Conclusion The results suggest that EGR 1 and BCL 2 protein involved in neuronal protection against ischemia,and EGR 1 may regulate the expression of bcl 2 gene.
关 键 词:脑缺血 海马 再灌注损伤 BCL-2基因 EGR-1基因
分 类 号:R743.310.2[医药卫生—神经病学与精神病学] R364.12[医药卫生—临床医学]
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