摘要
糖尿病肾病(diabetic nephropathy,DN)作为糖尿病的严重微血管并发症,已经成为导致终末期肾病的主要原因,严重危害人类健康。氧化应激及其持续伴随的炎症是糖尿病相关并发症的共同特征,也是DN进展的主要机制。核因子E2相关因子2(nuclear factor erythroid 2 related factor 2,Nrf2)通路被证实能够减少活性氧生成,并能够通过激活抗氧化级联反应来对抗炎症。因此,使用Nrf2靶向治疗来对抗DN中的氧化应激和炎症,对于DN具有明显的肾保护作用,能够降低尿蛋白,保护肾功能,改善肾纤维化,延缓DN进展。本文综述了有关Nrf2通路的最近研究进展,阐释了以Nrf2通路为靶点的有关DN肾的保护机制,以及Nrf2通路的调控和有关该通路激活药的研究,以期为进一步的基础研究提供方向,为发现DN有效治疗手段提供思路。
Diabetic nephropathy(DN),a serious microvascular complication of diabetes,has become the main cause of end-stage renal disease,seriously endangering human health.Oxidative stress and its persistent accompanying inflammation are common features of diabetes-related complications and major mechanisms of DN progression.Research in recent years has shown that the nuclear factor erythroid 2 related factor 2(Nrf2)pathwayhas been shown to reduce reactive oxide speciesproduction and to fight inflammation by activating the antioxidant cascade.Therefore,Nrf2-targeted therapy can combat oxidative stress and inflammation in DN to reduce urinary protein,protect renal function,improve renal fibrosis and delay the progression of DN,thus exerting renoprotective effect.This article reviews recent research progress on the Nrf2 pathway,illustrating the renoprotective mechanism targeting Nrf2 pathway,the regulation of Nrf2 pathway and researches on activators of this pathway in DN,in order to provide ideas for the basic research and the discovery of effective treatments for DN.
作者
李雅纯
刘利飞
陈志强
LI Ya-chun;LIU Li-fei;CHEN Zhi-qiang(Graduate School,Hebei University of Chinese Medicine,Shijazhuang 050091,Hebei Province,China;Traditional Chinese Medicine Hall,Hebei University of Chinese Medicine,Shijazhuang 050091,Hebei Province,China;Second Department of Nephrology,Hebei Hospital of Chinese Medicine,Shijiazhuang 050011,Hebei Province,China)
出处
《中国临床药理学杂志》
CAS
CSCD
北大核心
2022年第20期2497-2501,共5页
The Chinese Journal of Clinical Pharmacology
基金
国家自然科学基金资助项目(81373804)。
关键词
核因子E2相关因子2通路
糖尿病肾病
氧化应激
炎症
nuclear factor erythroid 2 related factor 2 signaling pathway
diabetic nephropathy
oxidative stress
inflammation