【目的】探讨具有癫痫基础病变小鼠在遭受颅脑损伤时,海马和顶叶皮质中C-FOS表达与损伤的相关性及其在损伤中的意义,为癫痫后颅脑损伤复合病变研究提供理论依据。【方法】用腹腔注射匹罗卡品法构建小鼠（2周龄）癫痫模型,饲养4周后（6周龄）采用自由落体法构建闭合性颅脑损伤小鼠模型和癫痫＋闭合性颅脑损伤小鼠模型,同时以正常小鼠为对照,于造模后0.5,3h及1,3,7d取小鼠大脑,制备切片,采用尼氏染色、免疫组织化学染色方法,从形态学以及蛋白质水平上研究各组小鼠大脑海马和顶叶皮质中C-FOS的表达情况。【结果】癫痫模型、闭合性颅脑损伤模型及癫痫＋闭合性颅脑损伤小鼠模型均构建成功。免疫组织化学染色结果显示,癫痫合并闭合性颅脑损伤小鼠顶叶皮质、海马均有着色深浅不同、数目不等的C-FOS阳性细胞。与对照组相比,单纯癫痫组、单纯闭合性颅脑损伤组、癫痫＋闭合性颅脑损伤组C-FOS灰度值均显著（P〈0.05）或极显著降低（P〈0.01）;癫痫＋闭合性颅脑损伤组小鼠海马和顶叶皮质C-FOS阳性细胞数均显著（P〈0.05）或极显著（P〈0.01）高于单纯癫痫组与单纯闭合性颅脑损伤组。【结论】癫痫小鼠颅脑损伤后,海马和顶叶皮质持续高表达C-FOS,从而促进神经细胞凋亡,加重颅脑损伤后的病理变化。%【Objective】 The study was done to elucidate the influences of epileptic brain on the expression of C-FOS following Traumatic Brain Injury（TBI）.【Method】 The status epilepticus of two-week-old mice were induced by a single i.p.injection of Pilocarpine.Fed for another 4 weeks（6 weeks） after the free fall method,a closed head injury mice model and epilepsy＋closed head injury model were constructed.Animals were then sacrificed 0.5,3 h and 1,3,7 d after TBI and the brains were processed for quantitative immunohistochemical of C-FOS in hippocampus and cortex.【Results】 Model of epilepsy,closed head injury and epilepsy model＋closed head injury in mice model were constructed successfully,immunohistochemical staining showed that the epilepsy associated with craniocerebral injury in mouse parietal cortex,the hippocampus had different coloring shades,not the number of the C-FOS-positive cells;with the blank control group,closed head injury group,simply head injury group,epilepsy,craniocerebral injury group,the C-FOS expression was significantly increased and maintained at a relatively high level（P〈0.05 or 0.01）;epilepsy,craniocerebral injuries mice hippocampus and parietal cortex C-FOS-positive cell counts were also significantly（P〈0.05） or highly significantly（P〈0.01） higher than the pure epilepsy group with closed traumatic brain injury alone group.【Conclusion】 Epilepsy the basis of lesions in mice brain injury,hippocampal,and parietal cortex sustained high expression of the C-FOS.Epilepsy lesions of brain damage,possibly through sustained high expression of the C-FOS to promote neuronal apoptosis,increased pathological changes after traumatic brain injury
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