The alleviation of oxidative damage in celiac disease by black soybean peptides and their mechanism.

BACKGROUND

Celiac disease (CD) is a chronic autoimmune condition that occurs in genetically predisposed individuals when they consume gluten. The α-gliadin peptide exacerbates the CD pathological process by inducing oxidative stress, intestinal cell damage, and apoptosis. Addressing oxidative stress in CD may offer a valuable strategy for supplementary treatment.

RESULTS

Black soybean peptides (BSPs) have been shown to inhibit oxidative stress and inflammation, although the specific mechanisms are not fully understood. This study investigated the effects of BSPs on Caco-2 cytotoxicity induced by the ɑ-gliadin peptide (p31-43). The p31-43 peptide significantly elevated reactive oxygen species (ROS) and malondialdehyde (MDA) levels in Caco-2 cells, disrupted the glutathione redox cycle, diminished antioxidant enzyme activity, and hampered the activation of antioxidant signaling pathways in a CD cell model. Pretreatment with BSPs inhibited the p31-43-induced increase in Keap1 protein levels, activated antioxidant genes through Nrf2, enhanced antioxidant enzyme activity, alleviated glutathione redox cycle imbalances, promoted catalytic subunit (GCLC) and regulatory subunit (GCLM) expression, and mitigated oxidative damage.

CONCLUSION

Black soybean peptides enhanced antioxidant defenses and mitigated p31-43-induced intestinal epithelial cell toxicity by modulating the Nrf2/Keap1 pathway, providing novel evidence for dietary intervention in CD. © 2026 Society of Chemical Industry.