创伤性脑损伤后NF-κBp65、ICAM-1表达及其意义

Expression and significance of nuclear factor-kappaBp65 and intercellular adhesion molecule-1 following experimental traumatic brain injury in rats

目的探讨核转录因子-κBp65亚单位(NF-кBp65)、细胞间粘连分子-1(ICAM-1)在大鼠急性创伤性脑损伤(TBI)后的表达变化规律及其意义。方法参照改良的Feeney自由落体脑损伤装置制备大鼠脑挫伤模型,分别于伤后6h、1、3、5、7d5个时间点取出脑组织,采用免疫组化染色和原位杂交方法,检测NF-кBp65、ICAM-1的活性变化。结果免疫组化结果显示:假手术组动物在任何存活时间点脑组织内均只能观察到很少的NF-κBp65、ICAM-1免疫反应;脑损伤后围绕损伤灶神经变性区,从伤后6h起,可观察到逐渐增加的NF-κBp65、ICAM-1免疫反应,伤后3d达到高峰(P<0.01)。原位杂交结果显示:假手术组动物脑组织内NF-κBp65、ICAM-1活性微弱;脑损伤后NF-κBp65、ICAM-1活性逐渐增强,伤后3d达到峰值(P<0.01)。结论创伤性脑损伤后NF-κBp65、ICAM-1的激活与脑炎性反应有关,是继发性脑损害的一个重要分子机制。

Objective To investigate the expression and significance of nuclear factor-kappaBp65 （NF-κBp65） and intercellular adhesion molecule-1 （ICAM-1） following experimental traumatic brain injury （TBI） in rats. Methods The model of local moderate brain contusion was established by the free-falling-body impact device according to the modified Feeney method. The activities of NF-κBp65 and ICAM-1 were detected by using the immunohistochemistry and in situ hybridization methods at 6 h, 1 d, 3 d, 5 d and 7 d respectively after TBI. Results The immunohistochemical results showed that the expressions of NF-κBp65 and ICAM-1 were low in the sham-operated group, while which increased from 6 h after TBI and reached the summit at 3 d （P 〈0.01 ）. The in situ hybridization results indicated that the activities of NF-κBp65 and ICAM-1 were weak in the sham-operated group, but which gradually reinforced at 6 h and reached the maximum at 3 d after TBI. Conclusion The activation of NF-κBp65 and ICAM-1 is related to brain inflammatory reaction, and which may be an important molecule mechanism of secondary brain injury after TBI.