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 (H2O2)‑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 H₂O₂ 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.