Detoxification stasis granules inhibit hepatocellular ferrozozois in mouse models of acute liver failure by enhancing GPX4 expression
Objective To investigate the potential mechanism of JDHY in the treatment of D-aminogalactose/lipopolysaccharide(D-GalN/LPS)-induced ALF in vitro.Methods Different concentrations of D-GalN/LPS were used to construct the ALF liv-er injury model,and different concentrations of JDHY drug-containing serum were co-cultured with the ALF liver damage mod-el,and the optimal concentration and co-culture time of JDHY were determined.Subsequently,the possible molecular mecha-nisms of JDHY were analyzed in vitro.Results Biochemical analysis and cell viability results showed that JDHY could effectively alleviate ALF hepatocyte injury.The results of iron ion concentration,MDA,Western blot and ELISA showed that JDHY could reduce the accumulation of unstable iron(Fe2+),alleviate lipid peroxidation,increase FTH1 protein,reduce TFR1 protein ex-pression,and inhibit ferroptosis and inflammatory expression levels(TNF-α,IL-6).The mechanism may be related to the fact that JDHY restored the metabolic activity of GSH/GPX4 and enhanced the antioxidant response,thereby inhibiting the process of LOX/PTGS pathway.Conclusion JDHY may promote the antioxidant activity of GSH/GPX4 by causing reprogramming of ALF hepatocytes,thereby inhibiting hepatocyte ferroptosis.
Detoxification and stasis granulesALFIron deathGPX4Oxidative stress
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