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Activation of antioxidant pathways, particularly the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway, by vitamin E represents a promising therapeutic strategy.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods and Results<\/jats:title>\n                    <jats:p>\n                      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\n                      <jats:inline-formula>\n                        <jats:tex-math>$$\\:\\text{\u03bc}$$<\/jats:tex-math>\n                      <\/jats:inline-formula>\n                      g\/mL liver extracellular matrix-derived hydrogel (LEMgel) from decellularized sheep liver. MASLD was induced by the co-culture treatment with Oleic acid (330 \u00b5M) and Palmitic acid (165 \u00b5M) for 2 days. Subsequently, cells were treated with 100\n                      <jats:inline-formula>\n                        <jats:tex-math>$$\\:\\text{\u03bcM}$$<\/jats:tex-math>\n                      <\/jats:inline-formula>\n                      vitamin E for 4 days. Oil Red O staining and gene expression analysis of\n                      <jats:italic>CD36<\/jats:italic>\n                      ,\n                      <jats:italic>SREBP-1c<\/jats:italic>\n                      , and\n                      <jats:italic>CPT-1<\/jats:italic>\n                      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\n                      <jats:italic>CPT-1<\/jats:italic>\n                      ,\n                      <jats:italic>NOX4<\/jats:italic>\n                      ,\n                      <jats:italic>SREBP-1c<\/jats:italic>\n                      ,\n                      <jats:italic>CD36<\/jats:italic>\n                      , and\n                      <jats:italic>PPAR<\/jats:italic>\n                      <jats:inline-formula>\n                        <jats:tex-math>$$\\:\\text{\u03b3}$$<\/jats:tex-math>\n                      <\/jats:inline-formula>\n                      , while upregulating\n                      <jats:italic>HO-1<\/jats:italic>\n                      ,\n                      <jats:italic>NQO1<\/jats:italic>\n                      ,\n                      <jats:italic>SOD<\/jats:italic>\n                      , and\n                      <jats:italic>GSH<\/jats:italic>\n                      , indicating enhanced antioxidant capacity. It also modulated hepatic markers (albumin, alpha-fetoprotein), suppressed LX-2 activation\n                      <jats:italic>via<\/jats:italic>\n                      TGF-\u03b2 inhibition, activated Nrf2 signaling, and induced expression of downstream target genes, including the antioxidant\/carboxylesterase gene CES1.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Overall, vitamin E attenuated oxidative stress and steatosis, and the biomimetic platform provides a physiologically relevant model for MASLD pathogenesis and drug screening.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1007\/s11033-026-12691-0","type":"journal-article","created":{"date-parts":[[2026,9,7]],"date-time":"2026-09-07T09:25:18Z","timestamp":1788773118000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Vitamin E treatment modulates steatotic and attenuates oxidative stress in a MASLD in vitro model"],"prefix":"10.1007","volume":"53","author":[{"given":"Seyedeh Kiana","family":"Teymoorian","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kosar","family":"Nouri","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mahmoud Alipour","family":"Choshali","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Moustapha","family":"Hassan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elham","family":"Rismani","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5924-4366","authenticated-orcid":false,"given":"Massoud","family":"Vosough","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Abbas","family":"Piryaei","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,9,7]]},"reference":[{"issue":"Suppl","key":"12691_CR1","doi-asserted-by":"publisher","first-page":"S32","DOI":"10.3350\/cmh.2024.0431","volume":"31","author":"ZM Younossi","year":"2024","unstructured":"Younossi ZM, Kalligeros M, Henry L (2024) Epidemiology of metabolic dysfunction-associated steatotic liver disease. 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