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苦参碱激活Nrf-2/HO-1信号通路并减轻高糖诱导的HK2细胞铁死亡。

Kurarinone activates the Nrf-2/HO-1 signaling pathway and alleviates high glucose-induced ferroptosis in HK2 cells.

作者信息

Ma Chunmei

机构信息

Department of Traditional Chinese Medicine, Jinan Central Hospital, No. 105 Jiefang Road, Jinan City, Shandong Province 250013, China.

出版信息

J Clin Biochem Nutr. 2025 Jul;77(1):30-36. doi: 10.3164/jcbn.24-210. Epub 2025 Apr 16.

Abstract

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.

摘要

为研究苦参酮对高糖(HG)刺激的HK2细胞铁死亡和上皮-间质转化(EMT)的可能影响,并揭示其机制。用葡萄糖处理HK2细胞以构建糖尿病肾病(DN)细胞模型。CCK-8和流式细胞术(FCM)检测显示其对HK2细胞生长和凋亡的影响。二氯荧光素(DCF)染色以及免疫印迹检测显示其对铁死亡的影响。JC-1染色显示其对线粒体功能的影响。免疫印迹检测显示其对HK2细胞EMT过程的影响。免疫印迹检测证实了该机制。苦参酮抑制HG刺激的HK2细胞凋亡。它还阻断HG刺激的HK2细胞铁死亡。进一步的数据表明,苦参酮抑制HG刺激的HK2细胞中线粒体损伤,并抑制EMT过程。机制上,苦参酮激活HG刺激的HK2细胞中的Nrf-2通路。苦参酮激活Nrf-2通路并减轻HG刺激的HK2细胞中的铁死亡和EMT。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7776/12326255/701a3c3808f5/jcbn24-210f01.jpg

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