Mulberroside A attenuates H

Abstract

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.

Key Findings

• Mulberroside A reduced oxidative stress levels in H2O2-induced Caco-2 cells.
• Mulberroside A improved intestinal epithelial barrier function by increasing transepithelial electrical resistance and tight junction protein expression.
• Mulberroside A promoted Nrf2 nuclear translocation and upregulated antioxidant enzymes HO-1 and NADPH quinone dehydrogenase 1, effects that were diminished by Nrf2 knockdown.

Clinical Significance

Citation

Chen Jianxin, Huang Xiufeng, Chen Xiet al.. Mulberroside A attenuates H Molecular medicine reports. 2026-Aug.