详细信息
Hedysarum polybotrys polysaccharide attenuates renal inflammatory infiltration and fibrosis in diabetic mice by inhibiting the HMGB1/RAGE/TLR4 pathway ( SCI-EXPANDED收录) 被引量:3
文献类型:期刊文献
英文题名:Hedysarum polybotrys polysaccharide attenuates renal inflammatory infiltration and fibrosis in diabetic mice by inhibiting the HMGB1/RAGE/TLR4 pathway
作者:Xu, Changqing[1];Chen, Yanxu[1];Liu, Zongmei[2];Fu, Xiaoyan[3]
第一作者:Xu, Changqing
通信作者:Fu, XY[1]
机构:[1]Gansu Univ Chinese Med, Clin Coll Tradit Chinese Med, Lanzhou 730000, Gansu, Peoples R China;[2]Shaanxi Univ Chinese Med, Clin Med Coll 1, Xianyang 710077, Shaanxi, Peoples R China;[3]Shaanxi Univ Chinese Med, Affiliated Hosp 2, Hyperbar Oxygen Chamber, 831 Longtaiguan Rd, Xian 710077, Shaanxi, Peoples R China
第一机构:甘肃中医药大学中医临床学院
通信机构:[1]corresponding author), Shaanxi Univ Chinese Med, Affiliated Hosp 2, Hyperbar Oxygen Chamber, 831 Longtaiguan Rd, Xian 710077, Shaanxi, Peoples R China.
年份:2023
卷号:26
期号:4
外文期刊名:EXPERIMENTAL AND THERAPEUTIC MEDICINE
收录:;WOS:【SCI-EXPANDED(收录号:WOS:001073749600001)】;
基金:Not applicable.
语种:英文
外文关键词:diabetic kidney disease; Hedysarum polybotrys polysaccharide; inflammatory; fibrosis; high mobility group box 1/receptor for advanced glycation endproducts/toll-like receptor 4 pathway
摘要:Diabetic kidney disease (DKD) is a leading cause of kidney failure. Previous studies demonstrated the therapeutic potential of Astragalus polysaccharide in treating diabetic nephropathy. Astragalus and Hongqi both come from the leguminous plant Astragalus, but their species and genera are different, belonging to the same family and different genera of traditional Chinese medicinal plants. However, the effects of Hedysarum polybotrys polysaccharide (HPS), a polysaccharide compound from Hongqi, on DKD, including its components and efficacy, have remained elusive. The present study utilized db/db mice as a DKD animal model administered with low (30 mg/kg) and high doses (60 mg/kg) of HPS, in addition to glyburide (7.2 mg/kg). Blood and urine samples were collected from mice and blood glucose, serum creatinine, urinary albumin excretion and urinary ss 2-microglobulin were measured. In addition, apoptosis and histological changes in kidney tissue were observed using TUNEL and HE staining, respectively, and the secretion and expression of inflammatory factors in kidney tissue were detected using EILSA and reverse transcription-quantitative PCR. Furthermore, we the expression of fibrosis-related proteins and NF-kappa B signaling pathway proteins was determined using western blot analysis. HPS was found to reduce the blood glucose concentration, serum creatinine levels, urinary albumin excretion rates and urinary ss 2-microglobulin in a dose-dependent manner. In addition, HPS treatment mitigated apoptosis and pathological damage in the kidney tissues of DKD mice. The expression levels of fibrosis-related proteins fibronectin, a-smooth muscle actin and TGF-ss 1 were observed to be decreased in kidney tissues of DKD mice following HPS treatment. The secretion levels of inflammatory factors (IL-6, TNF-alpha and IL-1 ss) were also reduced in kidney tissues, with high-dose HPS treatment found to be more effective, similar to the effects mediated by the glyburide. Further mechanistic analysis revealed that the therapeutic effects of HPS on DKD mice may be mediated by inhibiting the high mobility group box 1/receptor for advanced glycation end-products/toll-like receptor 4 pathway. In conclusion, the present findings could provide insight for the treatment of DKD.
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