The extract of Polygala fallax Hemsl. slows the progression of diabetic nephropathy by targeting TLR4 anti-inflammation and MMP-2/9-mediated anti-fibrosis in vitro

TLR4型 细胞凋亡 炎症 免疫印迹 糖尿病肾病 下调和上调 纤维化 促炎细胞因子 药理学 化学 生物 癌症研究 免疫学 医学 内分泌学 内科学 生物化学 基因
作者
Min Hui Wang,Xinyan Liu,Zelong Wang,Qin Xu
出处
期刊:Phytomedicine [Elsevier BV]
卷期号:104: 154251-154251 被引量:19
标识
DOI:10.1016/j.phymed.2022.154251
摘要

Polygala fallax Hemsl. is a plant that is commonly used as a folk medicine by Guangxi ethnic minorities, and it is also widely used in the clinical treatment of chronic diseases in China. The extract of P. fallax (EPF) contains key biologically active components from the roots and stems. However, the role of P. fallax or EPF in diabetic nephropathy (DN) is unclear.This study aimed to investigate the effects and mechanisms of EPF on high glucose (HG)-induced human glomerular mesangial cell (HMC) injury, inflammation, fibrosis, and apoptosis in vitro.For the in vitro study, MTT and ELISA assays were performed with HG-treated HMCs, as well as MMP, Hoechst, flow cytometry, qRT-PCR, and western blot analyses. The expression of the TLR4/NF-κB pathway, along with its downstream inflammatory, apoptosis, and fibrosis factors, was measured. The expression of the TLR4/NF-κB pathway and its downstream inflammatory factors were also measured after the addition of TLR4 inhibitors.Our results suggest that EPF can reverse the hyperproliferation and apoptosis of HMCs induced by HG. In addition, the extract inhibited the increase in inflammatory factors IL-6, TNF-α, IL-1β, MCP-1, and IL-18 in cells treated with HG. The mRNA and protein expression of TLR4, MyD88, NF-κB, Col IV, FN, MMP-9, and MMP-2 were downregulated by EPF. In addition, EPF significantly reduced the loss of MMP and the upregulation of Bcl-2/Bax mRNA and protein levels after HG treatment.These results demonstrated that EPF protects against diabetes-induced renal injury in vitro. EPF protected against HG-induced HMCs proliferation, apoptosis, fibrosis, and inflammation likely via inhibition of TLR4-dependent NF-κB signaling. This herbal extract may also be a novel treatment for DN.
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