Objective To explore the protective effect and mechanism of a compound staple food (CSF) against H₂O₂-induced oxidative damage in human hepatocellular carcinoma cells (HepG2).Methods The in vitro antioxidant capacity of CSF was evaluated using DPPH and ABTS radical scavenging assays. An oxidative stress model was established by inducing HepG2 cells with H₂O₂, and the effect of CSF on cell viability was measured by the CCK-8 assay. The impact of CSF on cellular oxidative stress was assessed by measuring reactive oxygen species (ROS), mitochondrial membrane potential (JC-1), malondialdehyde (MDA), and superoxide dismutase (SOD) levels. The effect of CSF on apoptosis was detected by flow cytometry. Expression changes of oxidative damage-related proteins (Nrf2, HO-1, NQO-1, Bax, and Bcl-2) were analyzed by Western blot.Results CSF effectively scavenged DPPH and ABTS radicals. Compared with the model group, CSF treatment increased the viability of H₂O₂-induced HepG2 cells, reduced ROS levels, slowed the decline of mitochondrial membrane potential, increased SOD activity, decreased MDA content, and alleviated Nrf2 nuclear translocation. CSF treatment reduced the apoptosis rate by 8% compared with the model group. Western blot results showed that CSF upregulated the expression of Nrf2, HO-1, and NQO-1, increased Bcl-2 levels, and downregulated Bax expression.Conclusion CSF improves H₂O₂-induced oxidative damage in HepG2 cells by activating the Nrf2/HO-1 pathway and regulating the Bcl-2/Bax pathway.