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在本实验中可见，随着供肝冷保存时间的延长，供肝中NFκB水平显著增高。其机制可能是随冷保存时间延长，内皮细胞和Kupffer细胞内氧自由基增多，低氧及氧化应激介导NFκB激活，调控TNFα、IL1β表达增高[11]。再灌注后各组肝组织中NFκB以及血清TNFα、IL1β水平均较冷保存期明显增高，并随着冷保存时间的延长活性增强。TUNEL显示肝细胞凋亡加重，反映肝损伤的酶学指标(ALT、AST)亦明显升高，表明再灌注后NFκB产生爆发式激活，转录大量TNFα、IL1β，进一步加重供肝的损伤。其机制可能与移植肝再灌注后呼吸爆发、氧化应激大大增强有关，而其转录产物如TNFα、IL1β又可进一步激活NFκB，形成正反馈。
可见，供肝的冷保存和再灌注是两个既独立又关联的过程。供肝的NFκB在冷保存期间就已经受到预激，并表达多种炎症介质，成为再灌注损伤的始动因子;在再灌注阶段NFκB的效应迅速放大，进一步激发并维持炎症反应，损伤供肝[12]。其中TNFα在肝损伤中发挥重要作用，可以直接或诱导肝细胞坏死、凋亡[13];而IL1β诱导Kuppfer细胞产生TNFα，上调中性粒细胞产生更多的自由基。二者的协同作用引起血管扩张和白细胞介导的组织坏死，最终导致器官衰竭。NFκB与细胞凋亡的关系密切, 其参与多种凋亡相关基因的转录调控, 具有抑制细胞凋亡作用及促细胞凋亡的双向作用，可能与不同亚基的转录有关，可以不通过炎性因子的作用，直接导致细胞凋亡[14]。在本实验中NFκB显示出促进肝细胞凋亡的作用。
总之，随着移植肝冷保存时间的延长，肝内NFκB存在不同程度的预激，再灌注后大量活化的NFκB通过上调TNFα、IL1β的表达直接或间接导致移植肝的损伤。这可能是移植肝再灌注损伤的重要机制，而抑制NFκB可能是一条减轻移植肝再灌注损伤的有效方法。
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