核因子-κB在缺血性脑损伤中作用机制的研究

The mechanisms of NF-κB in brain ischemic injury

目的 探讨核因子 -κBDNA(NF -κB)结合活性在缺血性脑损伤后的变化 ,及NF -κB在缺血性脑损伤中的作用。方法 采用四血管阻断法制作大鼠全脑缺血再灌注模型。采用EMSA法观察大鼠全脑缺血再灌注后海马CA1区NF -κBDNA结合活性变化。原位细胞凋亡检测法 (TUNEL染色 )及电镜观察脑缺血后CA1区神经原凋亡情况。结果 大鼠全脑缺血再灌后海马CA1区NF -κBDNA结合活性于再灌注 6h开始升高 ,再灌注 12h达高峰 ,再灌注 72h其结合活性仍保持一定水平 ,再灌注 7d其结合活性达对照组水平。再灌注 2 4h海马CA1区出现凋亡细胞 ,再灌注 72hCA1区凋亡细胞达高峰。结论 NF -κB参与了脑缺血再灌注损伤机制。NF

Objective To study the effects of NF-κB in brain ischemic injury by investigating the dynamic rule of NF-κB binding activity in CA1 region of rat hippocampus following global ischemia/reperfusion. Methods Transient cerebral ischemia was induced by 4-vessel occlusion (4-VO). The NF-κB binding activity was determined by EMSA after different periods of reperfusion. The apoptotic condition in the CA1 region after ischemia/reperfusion was studied in paraffin sections by using TUNEL method and electron microscopy. Results The activation of NF-κB in the CA1 region of hippocampus began to increase at 6 h of reperfusion, reached its peak level at 12 h, and began to decline gradually, being at a higher level at 72 h, until the 7d when the activation equaled to that in the sham-operation group. A few apoptotic cells were noticed 24 h after reperfusion (P<0.05). The number of them reached the peak level at 72 h (P<0.01) and began to decrease after reperfusion for 7 d (P<0.05). Conclusion NF-κB is involved in the process of brain ischemia/reperfusion injury, playing varied roles at different phases.