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目的观察大鼠颅脑外伤后生长相关蛋白(GAP-43)在中枢神经系统表达的变化,为探讨颅脑外伤后神经元再生和修复机制及临床应用药物治疗颅脑外伤提供理论依据。方法采用液压冲击法建立大鼠脑外伤模型,同时设正常对照组和假手术对照组。成模后取额皮质及海马部位,应用HE染色法观察额皮质区和海马CA1区的病理学改变,免疫组化法检测GAP-43的表达。结果轻、中、重度损伤组大鼠脑组织均出现明显的病理学改变,各损伤组大鼠创伤性颅脑外伤(TBI)后,额皮质区及海马CA1区均于12 h开始出现GAP-43表达增强,3 d后明显增强,1周达高峰,2周时开始降低。GAP-43的免疫反应产物的实际累积光密度值(CIOD)值在TBI 12 h后各时间点均明显高于同期的正常对照组和假手术对照组,中、重度损伤组CIOD值在TBI12 h后明显高于同期轻度损伤组。结论大鼠TBI后,GAP-43的表达增强;TBI损伤越重,其GAP-43的表达越强。
Objective To observe the changes of the expression of GAP-43 in central nervous system after craniocerebral trauma in rats and to provide a theoretical basis for exploring the mechanisms of neuronal regeneration and repair after craniocerebral trauma and the clinical application of drug-treated craniocerebral trauma. Methods The rat model of traumatic brain injury was established by hydraulic impact method. At the same time, normal control group and sham operation control group were established. The cortex and hippocampus were removed after modeling. The pathological changes of the frontal cortex and the hippocampal CA1 region were observed by HE staining. The expression of GAP-43 was detected by immunohistochemistry. Results The pathological changes of the brain tissue were observed in the mild, moderate and severe injury groups. After traumatic brain injury (TBI) in each injury group, both the frontal cortex and hippocampal CA1 region began to appear GAP- 43 expression increased significantly after 3 d, peaked at 1 week, 2 weeks began to decrease. The actual cumulative optical density (CIOD) value of GAP-43 immunoreactivity was significantly higher at 12h after TBI than that of the normal control group and the sham operation control group at the same time, and the CIOD value of moderate and severe injury group was significantly higher at TBI12h After being significantly higher than the same period mild injury group. Conclusion After TBI, the expression of GAP-43 is enhanced. The more severe TBI is, the stronger the expression of GAP-43 is.