摘要
目的 :从分子生物学水平 ,进一步深入研究颅脑创伤后神经细胞延迟性死亡的机制 ,探讨美洛宁对大鼠脑创伤后的影响 ,为临床治疗颅脑创伤提供一定的理论基础 .方法 :采用重型闭合性颅脑创伤模型 .利用免疫组化及原位凋亡检测 ,动态观察大鼠颅脑创伤后海马区p5 3蛋白的表达及神经细胞凋亡 .结果 :假手术组及正常对照组海马CA2区未检测出 p5 3蛋白的表达及凋亡阳性细胞 .创伤组大鼠伤后 3h海马CA2区出现 p5 3蛋白表达 ,2 4h (A =0 .14 9± 0 .0 16 )达高峰 ,72h即有所下降 ;伤后 2 4h ,海马CA2区即出现少量凋亡阳性细胞 ,于 16 8h (2 9.2± 4 .7/HP)达高峰 ,336h凋亡阳性细胞下降 .美洛宁组的 p5 3蛋白表达高峰 (A =0 .10 6±0 .0 17)及细胞凋亡的高峰 (2 1.0± 4 .6 /HP)较创伤组明显下调 .结论 :脑创伤后 p5 3蛋白表达增加可能造成神经细胞凋亡 ,美洛宁能够减少脑创伤后 p5 3蛋白表达 ,抑制神经细胞凋亡 .
AIM: To explore the mechanism of delayed neuronal death after traumatic brain injury (TBI) and probe into the effects of Cyclophosphamide (CTP) on rats after TBI. METHODS: The model of severe closed traumatic brain injury was used and the expression of p53 protein and nerve cell apoptosis in hippocampus were dynamically observed in rats after TBI by means of immunohistochemistry and TUNEL. RESULTS: The expression of p53 protein and apoptosis positive cells were not found in the hippocampus of the fake operation group and the normal group. The expression of p53 protein was found in the area of CA2 in hippocampus at 3 h after TBI in rats, which reached the peak at 24 h (A=0.149±0.016) and decreased at 72 h. Some apoptosis positive cells appeared in the area of CA2 in hippocampus in rats at 24 h after TBI, which reached the peak at 168 h (29.2±4.7/HP) and decreased at 336 h. The peak of the p53 protein ( A =0.106±0.017)expression and apoptosis(21.0±4.6/HP) in CTP group were obviously lower than those in TBI group. CONCLUSION: The increased expression of p53 protein may bring about nerve cell apoptosis after TBI. CTP can reduce the expression of p53 protein and restrain nerve cell apoptosis.
出处
《第四军医大学学报》
北大核心
2003年第18期1704-1706,共3页
Journal of the Fourth Military Medical University
关键词
脑
创伤
海马
P53
凋亡
胞苷三磷酸
brain
traumatic
hippocampus
p53
apoptosis
cyclophosphamide
