大鼠脑创伤后海马区Bax蛋白表达对神经细胞凋亡及学习记忆功能的影响

Effect of the expression of Bax protein in hippocampus on neural apoptosis and cognitive function after traumatic brain Injury in rats

①目的 探讨美洛宁对大鼠脑创伤后学习记忆功能的影响。②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,每组又分为伤后3、6、12、24、48、72、168及336h等8个时相组,每一时相组12只,另12只作为正常对照组。采用免疫组织化学、原位细胞凋亡检测,动态观察大鼠颅脑创伤后海马区的神经细胞凋亡,Bax蛋白的表达情况;另取48只大鼠随机分为脑创伤组、美洛宁治疗组、假手术组及正常对照组,进行水迷宫测试。③结果 脑创伤后海马区出现Bax蛋白表达增加,并出现神经细胞凋亡及学习记忆功能障碍。美洛宁治疗组海马神经细胞Bax蛋白表达高峰,及凋亡阳性细胞密度较创伤组有所下调,学习记忆功能改善。④结论 脑创伤后Bax蛋白表达增加可能造成伤后神经细胞凋亡和伤后学习记忆功能障碍,这是海马区神经细胞凋亡的必然结果,美洛宁能够减少脑创伤后Bax蛋白表达,并减少神经细胞凋亡,改善学习记忆功能。

Objective Certain theoretical bases are provided for clinical therapy on the basis of deeply studying mechanism of after traumatic brain injury and probing into the influences of cognitive function of CTP on rats after brain trauma. Methods The model of severe closed traumatic brain injury (TBI) was used. 300 Wistar rats were divided randomly into TBI group, CTP group and fake operation group and each of these three groups was divided into 8 subgroups, namely ,3,6, 12, 24, 48, 72, 168 and 336 hours. Each subgroup had 12 rats. At the same time, the rest 12 rats were taked as the normal group for comparison. Another 48 rats were divided randomly into 4 groups, namely, TBI group, CTP group, fake operation group and the normal group, and their cognitive dysfuction was evaluated using the Morris water maze ( MWM ) using such methods as immunohistochemistry and TUNEL stain, nerve cell apoptosis and the expression of Bax protein in hippocampus of rats after TBI were dynamically observed. Results The increased expression of Bax protein and neural apoptosis showed up in hippocampus and cognitive disfunction occurred after TBI. The peaks of Bax protein expression and nerve cell apoptosis in hippocampus of CTP group were lower than TBI group. But cognitive function was improved. Conclusions The increased expression of Bax protein may bring about nerve cell apoptosis after TBI. Cognitive function is inevitable outcome of nerve cell apoptosis in hippocampus. CTP can reduce the expression of Bax protein and nerve cell apoptosis and improve cognitive function.