Mulberroside A attenuates H2O2‑induced oxidative stress and barrier dysfunction in Caco‑2 cells through Nrf2/HO‑1‑associated antioxidant signaling

Within the present study, the aim was to investigate the impact of mulberroside A on hydrogen peroxide (H 2 O 2 )-induced oxidative stress and intestinal epithelial barrier dysfunction, as well as explore the involvement of nuclear factor erythroid 2-related factor 2 (Nrf2)-associated antioxidant signaling.Caco-2 cells were exposed to H 2 O 2 to establish an in vitro oxidative stress model.Cell viability, intracellular reactive oxygen species, lipid peroxidation, antioxidant enzyme activity, transepithelial electrical resistance and tight junction protein expression were assessed.Nrf2/heme oxygenase-1 (HO-1) pathway activation was evaluated using western blotting analysis and Nrf2 knockdown was used to examine pathway involvement.Results indicated that mulberroside A reduced oxidative stress levels, improved epithelial barrier function, promoted Nrf2 nuclear translocation and increased both HO-1 and NADPH quinone dehydrogenase 1 expression.These effects were attenuated following Nrf2 silencing.Overall, mulberroside A alleviated oxidative injury-associated intestinal epithelial barrier dysfunction in Caco-2 cells, supporting its potential relevance in oxidative stress-associated intestinal disorders.