Objective To investigate the effects of time-restricted feeding (TRF) on improving metabolic-associated steatohepatitis (MASH) and its underlying molecular mechanisms. 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 four groups: normal control (NC), normal time-restricted feeding (NT), model (M), and model time-restricted feeding (MT), with six mice per group. After 14 weeks of rearing, mice were anesthetized, weighed, 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 and the liver index was calculated. Oil red O, hematoxylin-eosin (HE), and Masson's trichrome staining were used to evaluate the degree of hepatic steatosis, inflammatory infiltration, and fibrosis. Protein expression levels of SIRT1, Nrf2, ACSL4, TfR1, SLC7A11, glutathione peroxidase 4 (GPX4), and tumor necrosis factor alpha (TNF-α) were detected by western blot. (2) An in vitro MASH model was established in HepG2 cells using oleic acid and cholesterol stimulation, and a fasting model was established via serum deprivation. The experimental cells were divided into the control group, serum-deprived (FBS-) group, M group, and M+FBS- group. The ferrostatin-1 (Fer-1) ferroptosis inhibitor was employed to investigate the relationship between ferroptosis and MASH/TRF. Sirt1 activity was inhibited using the Sirt1 inhibitor compound EX-527 to investigate the relationship between Sirt1 and Nrf2-mediated ferroptosis. Lipid accumulation in hepatocytes was observed via Oil Red O staining. HepG2 cell levels of TC, TG, ALT, and AST were measured using kits. Western blot analysis assessed the protein expression levels of Sirt1, Nrf2, TfR1, ACSL4, SLC7A11, GPX4, and TNF-α expression levels in HepG2 cells. Results (1) Compared with MASH mice, TRF significantly reduced body weight and serum levels of TC, TG, ALT, AST, MDA, and Fe2? (P < 0.01). Liver Fe2? levels and TNF-α expression were also markedly 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 TfR1 and ACSL4 protein levels in the livers of MASH mice (P < 0.01). (2) Compared with the M group, serum deprivation intervention reduced TC, TG, ALT, AST, MDA levels, and TNF-α expression in oleic acid-cholesterol-induced HepG2 cells (P < 0.01), effectively reducing the number of lipid droplets. Western blot analysis indicated that serum deprivation intervention markedly elevated Sirt1, Nrf2, SLC7A11, and GPX4 protein levels(P < 0.01) while markedly decreasing TfR1 and ACSL4 protein levels (P < 0.01). Following Fer-1 intervention, SLC7A11 and GPX4 protein levels markedly increased(P < 0.01), while TfR1 and ACSL4 protein levels effectively reduced (P < 0.01). Following EX-527 intervention, Sirt1, Nrf2, SLC7A11, and GPX4 protein levels substantially decreased(P < 0.05 or P < 0.01), while TfR1 and ACSL4 protein levels significantly increased(P < 0.01), markedly 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 metabolic-associated fatty liver disease by inhibiting ferroptosis, with its protective mechanism potentially involving the Sirt1/Nrf2 pathway it mediates.