Objective To investigate the effects of time-restricted feeding (TRF) on improving metabolicassociated steatohepatitis (MASH) and the underlying molecular mechanisms involved. Methods ( 1) A MASH model was established in C57BL / 6J mice using a high-fat, high-cholesterol diet. Twenty-four mice were randomly assigned to normal control ( NC), normal time-restricted feeding ( NT), model ( M), and model time-restricted feeding (MT) groups ( n=6 per group). Mice were anesthetized and weighed after 14 weeks, and serum samples were collected. Serum levels of total cholesterol ( TC), triglycerides ( TG), aspartate aminotransferase ( AST),alanine aminotransferase (ALT), malondialdehyde (MDA), and ferrous ions ( Fe²⁺) were measured. Livers were harvested to calculate the liver index. Oil Red O, hematoxylin-eosin (HE), and Masson’ s trichrome staining were used to evaluate hepatic steatosis degree, inflammatory infiltration, and fibrosis. Protein expression levels of silent information regulator 1 ( Sirt1), nuclear factor E2-related factor 2 ( Nrf2), acyl-coA synthetase long-chain family member 4( ACSL4), transferrin receptor 1 ( TfR1), solute carrier family 7 member 11 ( SLC7A11), glutathione peroxidase 4 (GPX4), and tumor necrosis factor alpha (TNF-α) were detected by Western blot. (2) Additionally,an in vitro MASH model was established in human HepG2 cells using oleic acid and cholesterol stimulation, and a fasting model was established with serum deprivation. Cells were divided into Control, serum-deprived (FBS-), M, and M + FBS- groups. The ferrostatin-1 ( Fer-1) ferroptosis inhibitor was employed to investigate the relationship between ferroptosis and MASH/ TRF. Sirt1 activity was inhibited using EX-527 to investigate the relationship between Sirt1 and Nrf2-mediated ferroptosis. Lipid accumulation in hepatocytes was observed with Oil Red O staining. HepG2 TC, TG, ALT, and AST levels were measured using kits. Western blot analysis was used to assess Sirt1, Nrf2,TfR1, ACSL4, SLC7A11, GPX4, and TNF-α protein expression levels in HepG2 cells. Results (1) Compared with MASH mice, TRF significantly reduced body weight and TC, TG, ALT, AST, MDA, and Fe²⁺ serum levels (P<0. 01). Liver Fe²⁺ levels and TNF-α expression were also decreased (P<0. 01), while hepatic steatosis and fibrosis were improved. Western blot analysis revealed that TRF intervention significantly increased Sirt1, Nrf2, SLC7A11,and GPX4 protein levels (P<0. 01) while decreasing those of TfR1 and ACSL4 in the livers of MASH mice (P<0. 01). (2) Compared with the M group, serum deprivation intervention reduced TC, TG, ALT, AST, MDA, and TNF-α levels in oleic acid-cholesterol-induced HepG2 cells ( P<0. 01), effectively reducing the number of lipid droplets. Western blot analysis indicated that serum deprivation elevated Sirt1, Nrf2, SLC7A11, and GPX4 protein levels ( P<0. 01) while decreasing those of TfR1 and ACSL4 ( P<0. 01). SLC7A11 and GPX4 protein levels increased following Fer-1 intervention (P<0. 01), while those of TfR1 and ACSL4 decreased (P<0. 01). Following EX-527 intervention, Sirt1, Nrf2, SLC7A11, and GPX4 protein levels decreased (P<0. 05 or P<0. 01), while TfR1 and ACSL4 levels significantly increased (P<0. 01), attenuating the ameliorative effects of serum deprivation on fat accumulation and injury in the M group ( P<0. 05 or P<0. 01). Conclusions TRF may improve metabolicassociated fatty liver disease by inhibiting ferroptosis, with its protective mechanism potentially involving Sirt1 / Nrf2 pathway mediation.