详细信息
Fucoidan from Laminaria japonica protects renal tubular epithelial cells from uric acid induced NLRP3-mediated pyroptosis through inhibition of NF-κB pathway ( SCI-EXPANDED收录) 被引量:3
文献类型:期刊文献
英文题名:Fucoidan from Laminaria japonica protects renal tubular epithelial cells from uric acid induced NLRP3-mediated pyroptosis through inhibition of NF-κB pathway
作者:Tan, Xiaohui[1];Zhang, Yu[1];Luo, Ping[1];Lin, Zhen[1];Li, Fangping[1];Liu, Huazhong[1]
机构:[1]Guangdong Ocean Univ, Coll Chem & Environm Sci, Zhanjiang 524088, Guangdong, Peoples R China
年份:2024
卷号:335
外文期刊名:JOURNAL OF ETHNOPHARMACOLOGY
收录:SCI-EXPANDED(收录号:WOS:001280479600001)、、Scopus(收录号:2-s2.0-85199314781)、WOS
基金:This work was supported by grants from Guangdong Basic and Applied Basic Research Foundation (No. 2022A1515012091) and Spe-cial Project in Key Fields of Guangdong Universities (No. 2022ZDZX2025) .
语种:英文
外文关键词:Fucoidan; Urate; NLRP3; Pyroptosis; HK-2 cell
外文摘要:Ethnopharmacological relevance: Hyperuricemia is a common metabolic disease with prominent morbidity, it can lead to many adverse effects and complications, such as chronic nephrosis. Fucoidan has been used as natural drug for acute and chronic kidney disease for over 20 years in China, but the precise mechanisms underlying the renal protective function are still indefinable. Purpose: This study is conducted to explore alleviation of fucoidan (FPS) from Laminaria japonica on urateinduced NOD-like receptor family, pyrin domain-containing 3 (NLRP3)-mediated pyroptosis in renal tubular epithelial cells HK-2, as well as the mechanism of nuclear factor kappa B (NF-kappa B) kappa B) signaling pathway involved. Materials and methods: HK-2 cells were treated with FPS, uric acid (UA), and inhibitor of NF-kappa B kappa B signaling pathway. Nitric oxide (NO) content and inducible nitric oxide synthase (iNOS) activity were determined with detection kits. Activation of intercellular NLRP3 inflammasome and NF-kappa B kappa B signaling pathway, gasdermin D (GSDMD) expression level were evaluated with Western blot and quantitative reverse transcription-PCR (qRTPCR), and immunofluorescent analysis. Results: Data showed that UA induced cellular inflammatory response demonstrated by elevated NO content, iNOS activity and expression level of NLRP3 inflammasome-mediated pyroptosis associated molecules including NLRP3, apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC), Caspase-1, interleukin 18 (IL-18) and GSDMD, moreover the NF-kappa B kappa B signaling pathway was activated by UA. However, FPS exposure inhibited efficiently the UA induced adverse effect. Conclusion: It can be concluded that FPS inhibited UA-induced NLRP3-mediated pyroptosis in HK-2 cells through repressing NF-kappa B kappa B signaling pathway.
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