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[The effect of nimesulide on learning and memory function after serve traumatic brain injury in rats].

Tao Zhang, Yuxin Zhang

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Abstract

OBJECTIVE: To investigate the effect of a cyclooxygenase-2 inhibitor nimesulide on learning and memory function of rats after traumatic brain injury (TBI). METHODS: 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). RESULTS: 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). CONCLUSION: Nimesulide may play a protective role on learning and memory function on severe traumatic brain injury of rats.

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OBJECTIVE: To investigate the effect of a cyclooxygenase-2 inhibitor nimesulide on learning and memory function of rats after traumatic brain injury (TBI). METHODS: 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). RESULTS: 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). CONCLUSION: Nimesulide may play a protective role on learning and memory function on severe traumatic brain injury of rats.

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Available abstract

OBJECTIVE: To investigate the effect of a cyclooxygenase-2 inhibitor nimesulide on learning and memory function of rats after traumatic brain injury (TBI). METHODS: 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). RESULTS: 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). CONCLUSION: Nimesulide may play a protective role on learning and memory function on severe traumatic brain injury of rats.

Key concepts: Nimesulide, Traumatic brain injury, Morris water navigation task, Medicine, Saline, Anesthesia, Western blot, Neurochemical

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