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Platycodin D regulates high glucose-induced ferroptosis of HK-2 cells through glutathione peroxidase 4 (GPX4)

Jinzhong Huang, Gangyi Chen, Jilei Wang, Shibin Liu, Jing Su

2022Bioengineered90 citationsDOIOpen Access PDF

Abstract

levels, and MDA levels and decreased GSH levels, suggesting that the HG condition induced ferroptosis. PD treatment inhibited ferroptosis in HG-induced cells, downregulated ACSL4 and TFR1 expression, and upregulated FTH-1 and SLC7A11 expression. PD reversed the effects of HG condition on cell death. Moreover, GPX4 expression was downregulated in HG-stimulated cells. Furthermore, we substantiated that PD suppressed ferroptosis by modulating GPX4 expression. In conclusion, PD inhibited ferroptosis in HG-induced HK-2 cells by upregulating GPX4 expression, suggesting that PD may be an effective drug for the clinical treatment of DN.

Topics & Concepts

GPX4Viability assayChemistryReactive oxygen speciesMalondialdehydeDownregulation and upregulationProgrammed cell deathMTT assayGPX1ApoptosisMolecular biologyGlutathioneOxidative stressGlutathione peroxidaseBiochemistryBiologyEnzymeGeneFerroptosis and cancer prognosisCancer, Lipids, and MetabolismCancer-related molecular mechanisms research
Platycodin D regulates high glucose-induced ferroptosis of HK-2 cells through glutathione peroxidase 4 (GPX4) | Litcius