Christman J W, Lancaster L H, Blackwell T S
Department of Medicine, Vanderbilt University School of Medicine and the Department of Veterans Affairs, Nashville, TN 37322-2650, USA.
Intensive Care Med. 1998 Nov;24(11):1131-8. doi: 10.1007/s001340050735.
NF-kappaB is an important transcription factor complex that appears to play a fundamental role in regulating acute inflammation through activation of the cytokine cascade and production of other pro-inflammatory mediators. There is increasing evidence that NF-kappaB is important in the pathobiology of disease states such as SIRS, MODS and ARDS; therefore, therapeutic interventions aimed at limiting NF-kappaB activation and down-regulating production of inflammatory mediators could prove to be beneficial in decreasing host-derived tissue injury and organ dysfunction. Specific interventions that hold promise for suppressing NF-kappaB activation include the use of antioxidants, inhibition of NIK and the IKK signalsome, treatment with proteasome inhibitors, induction of endotoxin tolerance and, possibly the use of corticosteroids in selected patients.
核因子-κB是一种重要的转录因子复合物，似乎在通过激活细胞因子级联反应和产生其他促炎介质来调节急性炎症中发挥着基础性作用。越来越多的证据表明，核因子-κB在全身炎症反应综合征、多器官功能障碍综合征和急性呼吸窘迫综合征等疾病状态的病理生物学中具有重要作用；因此，旨在限制核因子-κB激活并下调炎症介质产生的治疗干预措施可能有助于减少宿主源性组织损伤和器官功能障碍。有望抑制核因子-κB激活的具体干预措施包括使用抗氧化剂、抑制核因子诱导激酶和IκB激酶信号体、用蛋白酶体抑制剂治疗、诱导内毒素耐受以及在特定患者中可能使用皮质类固醇。
