Oxidative stress is caused by an imbalance of the antioxidant defense system and excessive production of free radicals, which can damage biological macromolecules such as proteins, lipids and nucleic acids, and can cause aging, ischemia-reperfusion injury, inflammatory injury, liver and kidney injury and other diseases. The nuclear factor erytheroid-2-related factor 2 (Nrf2) is a major regulator of redox balance. The Nrf2 pathway also exerts a central function in cell apoptosis, oxidative stress damage and metabolic diseases. Bioactive peptides are small molecular peptides composed of amino acid residues. They have many biological activities and play important physiological roles in human body. Antioxidant peptide is a kind of peptide which can reduce oxidative stress damage. They are safe, non-toxic and easily absorbed. In this review, we summarized the mechanism of bioactive peptides in regulating oxidative stress, especially antioxidant peptides, through regulating the Nrf2 signaling pathway and the expressions of oxidative stress-related genes, to alleviate oxidative stress-induced damage. The paper will provide valuable reference to investigators in the antioxidant peptide field and also promote the applications of antioxidant peptides in the oxidative stress-associated diseases.

Ulcerative colitis (UC) is a multifactorial, chronic inflammatory bowel disease with complex pathogenesis, posing significant challenges for therapeutic intervention. Barbaloin, a bioactive compound derived primarily from Aloe vera, exhibits diverse pharmacological properties, including anti-inflammation, anticancer, and organ-protective effects. This study comprehensively evaluated the anti-colitis function of barbaloin through in vivo and in vitro models. In the DSS-induced mouse colitis model, the administration of barbaloin significantly ameliorated disease severity, as confirmed by the reduced clinical and pathological damage. Notably, barbaloin restored gut microbiota homeostasis and increased beneficial bacterial genera (Akkermansia, Bacteroides, and Parabacteroides), while inhibiting the pathogenic Escherichia-Shigella. Serum metabolomics revealed changes in key metabolites such as 9-hpode and PE-NMe2 (22:6/14:1), indicating their involvement in lipid metabolism. Network pharmacology discovered that MAPK and NF-κB signaling pathways were potential targets for the action of barbaloin, and molecular docking and dynamics simulation showed that they had stable binding interactions. In vitro, barbaloin suppressed LPS-induced inflammation in RAW264.7 macrophages by inhibiting MAPK/NF-κB activation. Collectively, these findings elucidate a dual mechanism whereby barbaloin ameliorates colitis through microbiota-metabolite reprogramming and suppression of pro-inflammatory signaling, which provides a foundation for its development as a novel UC therapeutic agent.