Abstract Title:

Astragaloside IV ameliorates diabetic nephropathy inmice by inhibiting NLRP3 inflammasome‑mediated inflammation.

Abstract Source:

Int J Mol Med. 2021 Aug ;48(2). Epub 2021 Jul 19. PMID: 34278447

Abstract Author(s):

Hui Feng, Xiaoyun Zhu, Yang Tang, Shouqiang Fu, Bingtan Kong, Ximing Liu

Article Affiliation:

Hui Feng


Diabetic nephropathy (DN) is a primary cause of end‑stage renal disease. Despite the beneficial effects of astragaloside IV (AS)‑IV on renal disease, the underlying mechanism of its protective effects against DN has not been fully determined. The aims of the present study were to assess the effects of AS‑IV against DN inmice and to explore the mechanism of AS‑IV involving the NLR family pyrin domain containing 3 (NLRP3), caspase‑1 and interleukin (IL)‑1β pathways. The 8‑week‑oldmice received 40 mg/kg AS‑IV once a day for 12 weeks via intragastric administration. Cultured mouse podocytes were used to further confirm the underlying mechanism. AS‑IV effectively reduced weight gain, hyperglycemia and the serum triacylglycerol concentration inmice. AS‑IV also reduced urinary albumin excretion, urinary albumin‑to‑creatinine ratio and creatinine clearance rate, as well as improved renal structural changes, accompanied by the upregulation of the podocyte markers podocin and synaptopodin. AS‑IV significantly inhibited the expression levels of NLRP3, caspase‑1 and IL‑1β in the renal cortex, and reduced the serum levels of tumor necrosis factor (TNF)‑α and monocyte chemoattractant protein‑1. In high glucose‑induced podocytes, AS‑IV significantly improved the expression levels of NLRP3, pro‑caspase‑1 and caspase‑1, andinhibited the cell viability decrease in a dose‑dependent manner, while NLRP3 overexpression eliminated the effect of AS‑IV on podocyte injury and the inhibition of the NLRP3 and caspase‑1 pathways. The data obtained fromandexperiments demonstrated that AS‑IV ameliorated renal functions and podocyte injury and delayed the development of DN inmice via anti‑NLRP3 inflammasome‑mediated inflammation.

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