Kurarinone激活Nrf-2/HO-1信号通路,缓解高糖诱导的HK2细胞铁下垂。

IF 1.7 4区 医学 Q3 NUTRITION & DIETETICS
Journal of Clinical Biochemistry and Nutrition Pub Date : 2025-07-01 Epub Date: 2025-04-16 DOI:10.3164/jcbn.24-210
Chunmei Ma
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引用次数: 0

摘要

目的:探讨桂树酮对高糖(HG)刺激的HK2细胞铁下垂和EMT的可能影响,并揭示其机制。葡萄糖处理HK2细胞构建DN细胞模型。CCK-8和FCM实验显示了对HK2细胞生长和凋亡的影响。DCF染色和免疫印迹分析显示对铁下垂的影响。JC-1染色显示对线粒体功能的影响。免疫印迹分析显示了对HK2细胞EMT过程的影响。免疫印迹实验证实了其机制。Kurarinone抑制hg刺激的HK2细胞凋亡。它还能阻断hg刺激的HK2细胞的铁下垂。进一步的数据显示,Kurarinone抑制hg刺激的HK2细胞线粒体损伤,抑制EMT过程。在机械上,Kurarinone激活了hg刺激的HK2细胞中的Nrf-2通路。Kurarinone激活Nrf-2通路,减轻hg刺激的HK2细胞铁下垂和EMT。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Kurarinone activates the Nrf-2/HO-1 signaling pathway and alleviates high glucose-induced ferroptosis in HK2 cells.

To investigate the possible effects of Kurarinone on the ferroptosis and EMT of high glucose (HG)-stimulated HK2 cells, and uncover the mechanism. HK2 cells were treated with glucose to construct a DN cell model. CCK-8 and FCM assays exhibited the effects on growth as well as apoptosis of HK2 cells. DCF staining as well as Immunoblot assays exhibited the effects on ferroptosis. JC-1 staining exhibited the effects on mitochondrial function. Immunoblot assays showed the effects on the EMT process of HK2 cells. Immunoblot assays confirmed the mechanism. Kurarinone inhibited the apoptosis of HG-stimulated HK2 cells. It also blocked the ferroptosis of HG-stimulated HK2 cells. Further data showed that Kurarinone suppressed the mitochondrial damage in HG-stimulated HK2 cells, and restrained EMT process. Mechanically, Kurarinone activated the Nrf-2 pathway in HG-stimulated HK2 cells. Kurarinone activates the Nrf-2 pathway and alleviates HG-stimulated ferroptosis and EMT in HK2 cells.

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来源期刊
CiteScore
4.30
自引率
8.30%
发文量
57
审稿时长
6-12 weeks
期刊介绍: Journal of Clinical Biochemistry and Nutrition (JCBN) is an international, interdisciplinary publication encompassing chemical, biochemical, physiological, pathological, toxicological and medical approaches to research on lipid peroxidation, free radicals, oxidative stress and nutrition. The Journal welcomes original contributions dealing with all aspects of clinical biochemistry and clinical nutrition including both in vitro and in vivo studies.
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