Zhang Tao, Zhang Yu-Xin
Department of Neurosurgery, Xingtai People's Hospital, Hebei Medical University, Xingtai 054031, China.
Sichuan Da Xue Xue Bao Yi Xue Ban. 2011 Jul;42(4):498-502.
To investigate the effect of a cyclooxygenase-2 inhibitor nimesulide on learning and memory function of rats after traumatic brain injury (TBI).
The model of severe closed TBI was established according to the method created by Marmarou. Adult Wistar rats (n = 480) were randomly divided into TBI group, nimesulide treatment group, sham operation group, normal controls, and each of them was subdivided into posttraumatic 1, 3, 6, 12, 24, 48, 72, 96, 168, and 336 h groups. The nimesulide treatment group after injury was treated with nimesulide [6 mg/(kg x d)] in peritoneum. The TBI group, the sham operation group, and the control group were treated with normal saline. All rats were killed at each time point, COX-2 protein expression was evaluated with Western blot and immunohistochemistry. Another 24 rats were randomly divided into TBI group, nimesulide treatment group, sham operation group, and normal group. The cognitive dysfunction was evaluated using the Morris water maze (MWM).
The increased expression of protein COX-2 in brain after TBI was observed. A significantly decreased peak of COX-2 protein expression was observed in nimesulide treated group when compare with that of TBI (P < 0.05). An significant shorter latency of MWM tests at 9,10 days after nimesulide treatment was also observed (P < 0.01).
Nimesulide may play a protective role on learning and memory function on severe traumatic brain injury of rats.
探讨环氧化酶-2抑制剂尼美舒利对创伤性脑损伤（TBI）大鼠学习记忆功能的影响。
按照Marmarou创建的方法建立重度闭合性TBI模型。成年Wistar大鼠（n = 480）随机分为TBI组、尼美舒利治疗组、假手术组、正常对照组，每组再分为伤后1、3、6、12、24、48、72、96、168和336 h组。伤后尼美舒利治疗组给予腹腔注射尼美舒利[6 mg/(kg·d)]。TBI组、假手术组和对照组给予生理盐水。在各个时间点处死所有大鼠，采用蛋白质免疫印迹法和免疫组织化学法评估COX-2蛋白表达。另取24只大鼠随机分为TBI组、尼美舒利治疗组、假手术组和正常组。采用Morris水迷宫（MWM）评估认知功能障碍。
观察到TBI后大鼠脑内COX-2蛋白表达增加。与TBI组相比，尼美舒利治疗组COX-2蛋白表达峰值明显降低（P < 0.05）。尼美舒利治疗后第9、10天MWM试验潜伏期也明显缩短（P < 0.01）。
尼美舒利可能对大鼠重度创伤性脑损伤的学习记忆功能起保护作用。
