尼莫同对大鼠创伤性脑损伤后脑组织NF—κB表达和活化的影响

Effect of nimotop on expression and activation of NF-κB in the rat brain tissues after traumatic brain injury

目的观察尼莫同对大鼠创伤性脑损伤（traumatic brain injury，TBI）后NF-κB表达和活化的影响。方法制作SD大鼠落体撞击脑损伤模型，分别给予地塞米松和尼莫同干预，检测脑组织NF—κB P65和IκBα的表达。结果TBI后腑组织NF—κB P65的表达明显增加，伤后24h最低，持续到96h仍有明显表达；IκBa表达明显减弱，伤后24h达到低峰。尼莫同与地塞米松可以显著降低TBI后NF—κBP65的表达和增加IκBa的表达（P〈0．01），尼莫同作用优于地塞米松（P〈0．05）。结论尼莫同可以抑制TBI后NF—κB表达和活化，从而调节脑损伤后的炎症反应。

Objective To explore the effect of nimotop on expression and activation of NF-κB after traumatic brain injury. Methods Local traumatic brain injury was made in rats by strike with free-falling hammer. Then, the rats were injected with dexamethasone and nimotop respectively to detect expressions of NF-κB P65 and IκBα in rat brain tissues by means of immunohistochemistry. Results The expression of NF-κB P65 in brain tissue was obviously increased after traumatic brain injury and reached peak at 24 hours, which lasted for 96 hours. The expression of IKB was obviously decreased after traumatic brain injury and lowered to the least at 24 hours. Both dexamethasone and nimotop could decrease the expression of NF-κB P65 and increase the expression of IκBα in rat brain tissues after traumatic brain injury （ P 〈 0.01 ）, when nimotop was better than dexamethasone （ P 〈 0.05）. Conclusions Nimotop can inhibit the expression and activation of NF-κB and hence regulate inflammatory reaction after traumatic brain injury.