NF?κB是近年发现的与缺血性脑损伤后脑组织中免疫应答反应密切相关的转录因子。许多研究表明，脑缺血时神经细胞、脑血管内皮细胞和胶质细胞中均有NF?κB的活化[15]，多种因素如细胞因子、氧化剂、缺血等均是NF?κB活化的刺激信号，NF?κB活化后可促进粘附分子、立早基因、细胞表面受体和细胞因子的基因表达，进一步加重脑缺血过程的炎症反应。越来越多的证据显示，NF?κB的激活是炎症反应的关键和焦点，与脑缺血及再灌注损伤时的炎症机制密切相关。由于NF?κB在缺血性脑损伤炎性反应中的中心作用，NF?κB有望成为治疗缺血性脑血管病新的药理学靶点，为脑缺血的临床治疗提供了新的思路。
本实验显示ND?308能够改善脑缺血再灌注大鼠神经行为学障碍，减小脑梗死体积，改善缺血组织形态学变化，能够减少缺血组织中IL?1β、TNF?α、NF?κB的表达及抑制NF?κB向细胞核内转运，对缺血脑组织损伤有明显保护作用，其机制可能与抑制炎症因子表达有关。
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