Mulberroside A attenuates H<sub>2</sub>O<sub>2</sub>‑induced oxidative stress and barrier dysfunction in Caco‑2 cells through Nrf2/HO‑1‑associated antioxidant signaling

Chen,Jianxin; Huang,Xiufeng; Chen,Xi; Jin,Wenhai; Lin,Dawei

doi:10.3892/mmr.2026.13946

August-2026 Volume 34 Issue 2

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August-2026 Volume 34 Issue 2

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Article Open Access

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

Authors:
- Jianxin Chen
- Xiufeng Huang
- Xi Chen
- Wenhai Jin
- Dawei Lin
View Affiliations / Copyright

Affiliations: Second Department of Gastrointestinal Surgery, Affiliated Hospital of Putian University, Putian, Fujian 351100, P.R. China

Copyright: © Chen et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
Article Number: 236
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Published online on: June 25, 2026

https://doi.org/10.3892/mmr.2026.13946
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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.

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