文献类型：期刊文献

英文题名：Hedysarum polysaccharide alleviates oxidative stress to protect against diabetic peripheral neuropathy via modulation of the keap1/Nrf2 signaling pathway

作者：He, Liu[1,3];Huan, Pengfei[2,3];Xu, Jing[1];Chen, Yanxu[3];Zhang, Lei[3];Wang, Jun[3];Wang, Li[1,2,4];Jin, Zhisheng[3]

第一作者：He, Liu;何黎;何玲

通信作者：Wang, L[1];Jin, ZS[2]

机构：[1]Guizhou Univ Tradit Chinese Med, Affiliated Hosp 2, Guiyang 550005, Peoples R China;[2]Shanghai Univ Tradit Chinese Med, Sch Basic Med, Dept Diagnost Tradit Chinese Med, Shanghai 201203, Peoples R China;[3]Gansu Univ Chinese Med, Lanzhou 730000, Peoples R China;[4]Shanghai Univ Tradit Chinese Med, Shanghai Municipal Hosp Tradit Chinese Med, Expt Ctr, Shanghai 200071, Peoples R China

第一机构：Guizhou Univ Tradit Chinese Med, Affiliated Hosp 2, Guiyang 550005, Peoples R China

通信机构：[1]corresponding author), Guizhou Univ Tradit Chinese Med, Affiliated Hosp 2, Guiyang 550005, Peoples R China;[2]corresponding author), Gansu Univ Chinese Med, Lanzhou 730000, Peoples R China.|[10735]甘肃中医药大学;

年份：2022

卷号：126

外文期刊名：JOURNAL OF CHEMICAL NEUROANATOMY

收录：;Scopus(收录号：2-s2.0-85143280155);WOS:【SCI-EXPANDED(收录号:WOS:000901483800002)】；

基金：Acknowledgments The study was supported by grants from the National Natural Science Foundation of China (No. 81660777) and the Youth Science Fund Project of National Natural Science Fund of China (No. 82104965) .

语种：英文

外文关键词：Oxidative stress; Hedysarum polysaccharide; Diabetic peripheral neuropathy; Keap1; Nrf2 pathway

摘要：Diabetic peripheral neuropathy (DPN) is a chronic complication of diabetes mellitus. Oxidative stress is implicated in DPN progression, suggesting that antioxidant therapy could be a viable anti-DPN method. Hedysarum polysaccharide (HPS) is an active component of Radix Hedysari, a plant that has been widely used as food and a herb for treating multiple diseases. Here, we evaluated the mechanisms of action of anti-DPN effects of HPS in genetically obese (ob/ob) mice. Schwann cells (SCs) were exposed to glucose (100 mM) in vitro and then treated with HPS at concentrations of 30, 60, 120, and 240 mg/L. Notably, HPS significantly inhibited high glucosemediated cytotoxicity and oxidative stress by reducing malondialdehyde (MDA) levels and upregulating the expression of antioxidant enzymes (gamma-glutamate-cysteine ligase catalytic subunit (GCLC) and glutathione reductase (GR)) in SCs. Moreover, HPS increased the expression of nerve growth factor, stimulated Nrf2 signaling, and decreased Keap1 expression levels. Analysis of DPN mice models gavaged with HPS at 50, 100, and 200 mg/kg/d or lipoic acid (LA) at 30 mg/kg/d (positive control) for 8 weeks revealed that HPS markedly increased motor nerve conduction velocity (MNCV), shortened thermal withdrawal latency (TWL), and inhibited oxidative stress in serum and sciatic nerves of DPN mice models. Mechanistically, HPS suppressed Keap1 signaling and enhanced Nrf2 signaling in sciatic nerves. These findings imply that HPS ameliorates DPN via antioxidant mechanisms and by activating Keap1/Nrf2 signaling, suggesting that HPS is a potential treatment option for DPN.