论文部分内容阅读
目的：探讨脑局部缺血后神经元损伤的分子机制。方法：经颞骨开窗结扎大鼠大脑中动脉，制成脑局部缺血模型，采用地高辛标记Ｃ－ｆｏｓ探针原位杂交法，观察脑缺血后大脑皮层及海马等区域Ｃ－ｆｏｓ基因的表达状况，用Ｃ－ｆｏｓ阳性细胞密度作定量研究指标。结果：脑缺血组、氯胺酮组和对照组，在大脑皮层及海马区域Ｃ－ｆｏｓ阳性细胞分别呈高密度、低密度和散在分布，三组间相差显著（Ｐ＜０．０１）。在脑的其余部位，包括丘脑、脑干、小脑等区域，三组Ｃ－ｆｏｓ阳性细胞均呈散在分布，无组间差异。结论：脑局部缺血可诱发大脑皮层及海马Ｃ－ｆｏｓ基因表达，Ｃ－ｆｏｓ基因表达可能是缺血致神经元损伤的分子机制之一；氯胺酮对脑缺血后Ｃ－ｆｏｓ基因表达有部分抑制作用；ＮＭＤＡ受体激活可能参与了缺血后Ｃ－ｆｏｓ基因表达过程
Objective: To investigate the molecular mechanism of neuronal damage after cerebral ischemia. Method: The rat brain ligated artery temporal bone window, made ischemic brain model, using digoxigenin labeled C-fos probe in situ hybridization was observed after cerebral ischemia in cortex and hippocampus etc. regions C-fos Gene expression, using C-fos positive cell density for quantitative research indicators. Results: The C-fos positive cells in cerebral cortex and hippocampus of cerebral ischemic group, ketamine group and control group showed high density, low density and scattered distribution respectively, with significant difference between the three groups (P <0.01). The rest of the brain, including the thalamus, brain stem, cerebellum and other regions, three groups of C-fos positive cells were scattered, no differences between groups. Conclusion: Cerebral ischemia can be induced in cortex and hippocampus C-fos gene expression, C-fos gene expression may be induced by one of the molecular mechanisms of ischemic neuronal damage; ketamine part of the C-fos gene expression after cerebral ischemia Inhibition; NMDA receptor activation may be involved in the post-ischemic C-fos gene expression process