大鼠脑创伤后海马区Fas蛋白表达与神经细胞凋亡

目的进一步深入研究颅脑创伤后神经细胞凋亡的机制,探讨美洛宁对大鼠脑创伤后的影响,为临床治疗颅脑创伤病人提供一定的理论基础.方法采用重型闭合性颅脑创伤模型,将Wistar大鼠300只随机分为脑创伤组、美洛宁治疗组、假手术组,每组又分别划分成伤后3、6、12、24、48、72、168及336 h等8个时相组,每时相组各12只,另12只作为正常对照组.动态观察大鼠颅脑创伤后海马区的神经细胞凋亡以及Fas蛋白的表达情况.结果脑创伤后海马区出现Fas蛋白表达增加并出现神经细胞凋亡.美洛宁治疗组伤后海马神经细胞Fas蛋白表达高峰较创伤组明显下调,凋亡阳性细胞密度亦较创伤组有所下调.结论脑创伤后Fas蛋白表达增加可能造成伤后神经细胞凋亡,美洛宁能够减少脑创伤后Fas蛋白表达,并减少神经细胞凋亡.

Effects of Fas protein expression on neural apoptosis in hippocampus after traumatic brain injury in rats

Objective To study the mechanisms of nerve cell apoptosis after traumatic brain injury and the influences of CTP on rats after brain trauma. Methods The model of severe closed traumatic brain injury (TBI) was used. A total of 300 Wistar rats were divided randomly into TBI group, CTP treatment group, and sham operation group. The Fas protein expression and neural apoptosis in each group were observed at 3, 6, 12, 24, 48, 72, 168, and 336 h after TBI. At the same time, the rest 12 rats were employed as the normal controls. Immunohistochemistry and TUNEL staining were used to observe the neural apoptosis and the expression of Fas protein in hippocampus of rats after TBI. Results Increased expression of Fas protein and neural apoptosis were found in the rat hippocampus after TBI. Conclusion The increased expression of Fas protein may result in neural apoptosis after TBI. CTP can reduce the expression of Fas protein and neural apoptosis.