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机构地区:[1]山西省人民医院神经外科,太原030012 [2]上海第二医科大学附属宝钢医院
出 处:《中华急诊医学杂志》2003年第11期739-741,T001,共4页Chinese Journal of Emergency Medicine
摘 要:目的 探讨颅脑损伤后神经细胞凋亡分子的病理机制 ,为临床防治提供实验依据。方法 采用免疫组织化学技术和原位末端标记法 (TUNEL)检测大鼠伤灶边缘皮层的fos蛋白及凋亡细胞。结果 外伤组在伤后 2 4h检测到高水平表达的fos蛋白及明显增多的凋亡神经细胞。结论 外伤后fos表达参与诱导了神经细胞凋亡过程。Objective To explore the pathologic mechanism of nerve cell apoptosis after traumatic brain injury at gene level,and to provide some theoretical guide for clinical therapy.Methods Male Sprague-Dawley rats were divided into two gorups at random:control group and truama group.Immunohistochemistry and terminal deoxynucleotidyl transferase-mediated biotinylated-deoxyuridine triphosphate nick-end labeling technique were used to detect the fos protein and the apoptotic cells in the septal ipsilateral cerrebral cortex at different phrases after injury.Results The level of fos protein and apoptotic cells were observed at 24h after injury in trauma group,but only few fos protein and apoptotic cells existed in the control group.Conclusion The delayed-expression of C-fos gene after injury may induce nerve cell apotosis in early stage.
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