核因子κB抑制物在糖尿病周围神经病变中的研究进展  

Role of the Nuclear Factor Kappa B Inhibitors in the Pathological Changes of Diabetic Peripheral Neuropathy

作　　者：唐佳雯[1] 朱涛[2] TANG Jiawen ZHU Tao(Nanjing Medical University, Nanjing 210029, China Department of Anesthesiology, Shanghai Songjiang Center Hospital, Shanghai 201600, China)

机构地区：[1]南京医科大学,南京210029 [2]上海市松江区中心医院麻醉科,上海201600

出　　处：《医学综述》2017年第8期1613-1617,共5页Medical Recapitulate

基　　金：上海市科研计划项目(134119b2700)

摘　　要：对于糖尿病周围神经病变(DPN),目前只是对症治疗,还没有具体的预防或治疗措施。而炎症参与了DPN的发生、发展且涉及一个复杂的分子网络和过程。在DPN动物模型和临床试验中,抗炎药物的应用逐渐受到重视。且Toll样受体4、核因子κB(NF-κB)、NF-κB抑制剂蛋白和NF-κB抑制剂激酶等髓样分化蛋白88依赖型/非依赖型信号通路中的关键蛋白分子也参与了DPN的病程进展,其中NF-κB主要调控炎症反应。可见,使用NF-κB抑制物对于减缓DPN有重要作用,通过抑制NF-κB炎症信号通路来缓解糖尿病神经病理病变可能是未来治疗DPN的一个新方向。Current treatment for diabetic peripheral neuropathy （DPN） is only symptomatic rather than preventive or therapeutic. Inflammation can cause and aggregate DPN by complex molecular network. More and more anti-inflammatory drugs have got recognition in animal and clinical trials of DPN. And Toll like receptor 4, nuclear factor kappa B （NF-κB） , inhibitor of NF-κB proteins, and inhibitor of NF-κB kinases myeloid differentiation protein 88 dependent/independent key protein type signaling pathway is also involved in the course of DPN. NF-κB subunits modulate the inflammation reaction. It is found that NF-κB inhibitors play an important role in the mitigation of DPN. It might be a new way to treat DPN in the future by inhibiting the inflammatory signal pathway of NF-κB in order to relieve the pathological changes of DPN.

关 键 词：糖尿病周围神经病变 核因子ΚB 核因子κB抑制剂蛋白 核因子κB抑制剂激酶 TOLL样受体4 

分 类 号：R587.2[医药卫生—内分泌]