中国临床药理学杂志2024,Vol.40Issue(2) :284-288.DOI:10.13699/j.cnki.1001-6821.2024.02.028

中药活性成分调控Nrf2/HO-1信号通路防治糖尿病肾病的研究现状

Research status on the regulation of Nrf2/HO-1 signaling pathway by active ingredients of Chinese medicine in the prevention and treatment of diabetic kidney disease

聂宵 王志刚 梁永林
中国临床药理学杂志2024,Vol.40Issue(2) :284-288.DOI:10.13699/j.cnki.1001-6821.2024.02.028

中药活性成分调控Nrf2/HO-1信号通路防治糖尿病肾病的研究现状

Research status on the regulation of Nrf2/HO-1 signaling pathway by active ingredients of Chinese medicine in the prevention and treatment of diabetic kidney disease

聂宵 1王志刚 2梁永林3
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作者信息

  • 1. 甘肃中医药大学中医临床学院,甘肃兰州 730000
  • 2. 天水市中医医院内分泌科,甘肃天水 741099
  • 3. 甘肃中医药大学基础医学院,甘肃兰州 730000
  • 折叠

摘要

糖尿病肾病(DKD)是由糖尿病(DM)引起的一种高发的微血管并发症,持续的高糖使机体产生氧化应激反应,核转录因子E2相关因子2/血红素加氧酶-1(Nrf2/HO-1)能够通过抑制肾小球系膜细胞外基质的积累、抑制肾小管上皮细胞发生上皮-间充质转化、抑制铁凋亡等途径发挥抗炎抗氧化作用,改善肾功能的损伤,延缓DKD的进程.本文从Nrf2/HO-1通路及其相关因子着手,对Nrf2/HO-1通路与DKD的关系以及中药活性成分通过Nrf2/HO-1信号通路对DKD的影响作一综述,以期为新药的开发提供依据.

Abstract

Diabetic kidney disease(DKD)is a high incidence microvascular complication caused by diabetes mellitus(DM).Persistent high glucose induces oxidative stress in the body.nuclear factor erythroid 2-related factor 2/heme oxygenase-1(Nrf2/HO-1)can play an anti-inflammatory and anti-oxidative role by inhibiting the accumulation of extracellular matrix in glomerular mesangium,inhibiting epithelial-mesenchymal transition in renal tubular epithelial cells,and inhibiting iron apoptosis,so as to improve renal function damage and delay the process of DKD.This article reviews the relationship between Nrf2/HO-1 pathway and DKD and the effect of traditional Chinese medicine active ingredients on DKD through Nrf2/HO-1 signaling pathway,in order to provide a basis for the development of new drugs.

关键词

中药活性成分/糖尿病肾病/核转录因子E2相关因子2/血红素加氧酶-1

Key words

active ingredients of traditional Chinese medicine/diabetic kidney disease/nuclear factor erythroid 2-related factor 2/heme oxygenase-1

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基金项目

甘肃省教育厅产业支撑计划(2021CYZC-03)

出版年

2024
中国临床药理学杂志
中国药学会

中国临床药理学杂志

CSTPCDCSCD北大核心
影响因子:1.91
ISSN:1001-6821
被引量1
参考文献量13
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