Molecular biology reports · 2026
Vitamin E treatment modulates steatotic and attenuates oxidative stress in a MASLD in vitro model.
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Teymoorian Seyedeh Kiana, Nouri Kosar, Choshali Mahmoud Alipour, Hassan Moustapha, Rismani Elham, Vosough Massoud, Piryaei Abbas
Аннотация
BACKGROUND: Metabolic 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 RESULTS: In 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.
CONCLUSIONS: Overall, vitamin E attenuated oxidative stress and steatosis, and the biomimetic platform provides a physiologically relevant model for MASLD pathogenesis and drug screening.
METHODS AND RESULTS: In 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.
CONCLUSIONS: Overall, vitamin E attenuated oxidative stress and steatosis, and the biomimetic platform provides a physiologically relevant model for MASLD pathogenesis and drug screening.