ArticleMolecular biology reports2026
Vitamin E treatment modulates steatotic and attenuates oxidative stress in a MASLD in vitro model.
Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundMetabolic dysfunction-associated steatotic liver disease (MASLD) is a major chronic liver disorder and a growing global health concern driven in part by oxidative stress. Activation of antioxidant pathways, particularly the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway, by vitamin E represents a promising therapeutic strategy. METHODS AND
resultsIn this study, we developed a biomimetic co-culture platform to evaluate the impact of vitamin E on oxidative stress and steatosis progression in a MASLD model. The model consisted of a co-culture of Huh-7 and LX-2 cells (4:1) seeded on plates coated with 100 [Formula: see text]g/mL liver extracellular matrix-derived hydrogel (LEMgel) from decellularized sheep liver. MASLD was induced by the co-culture treatment with Oleic acid (330 µM) and Palmitic acid (165 µM) for 2 days. Subsequently, cells were treated with 100 [Formula: see text] vitamin E for 4 days. Oil Red O staining and gene expression analysis of CD36, SREBP-1c, and CPT-1 confirmed successful steatosis induction and transcriptome alterations consistent with a MASLD phenotype. Vitamin E treatment significantly improved cell viability, reduced intracellular lipid accumulation, and downregulated CPT-1, NOX4, SREBP-1c, CD36, and PPAR[Formula: see text], while upregulating HO-1, NQO1, SOD, and GSH, indicating enhanced antioxidant capacity. It also modulated hepatic markers (albumin, alpha-fetoprotein), suppressed LX-2 activation via TGF-β inhibition, activated Nrf2 signaling, and induced expression of downstream target genes, including the antioxidant/carboxylesterase gene CES1.
conclusionsOverall, vitamin E attenuated oxidative stress and steatosis, and the biomimetic platform provides a physiologically relevant model for MASLD pathogenesis and drug screening.
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