Prevention and potential repair of colitis: Beneficial effects and regulatory mechanisms of food-derived anti-inflammatory peptides.

Intestinal inflammatory diseases are increasingly prevalent worldwide, and their pathogenesis is still not fully understood. As of late, studies have discovered that food-derived peptides have specific anti-inflammatory activity and can play a positive role in intestinal health. At the same time, it has broad application prospects in the prevention and treatment of colitis because of its wide source, fast absorption, and high safety. This article reviews the structure-activity and quantity-effect relationships of food-derived peptides for their anti-inflammatory effects. It then discusses their mechanism of action in inhibiting colitis from four aspects. Food-derived anti-inflammatory peptides can delay the progression of the disease by stimulating innate immunity, inhibiting inflammation, and promoting wound healing. Further experiments showed that food-derived anti-inflammatory peptides could prevent and treat colitis through four mechanisms: (a) regulation of inflammatory cytokines; (b) regulation of inflammatory pathways; (c) regulation of intestinal epithelial barrier; (d) regulation of intestinal flora balance. However, due to the treatment of colitis having limitations, there is an urgent to develop food-derived anti-inflammatory peptides as a treatment or adjunctive treatment for colitis. This review highlights the positive effects of food-derived peptides on colitis and anticipates the appearance of mitigating peptides for the therapy of colitis.

Tricholoma matsutake-Derived Peptides Show Gastroprotective Effects against Ethanol-Induced Acute Gastric Injury.

Acute gastric injury caused by ethanol is a frequent disorder of the gastrointestinal tract. In this study, we investigated the potential gastroprotective effects of Tricholoma matsutake-derived peptides against ethanol-triggered acute gastric injury and the associated mechanisms. Peptides SDLKHFPF and SDIKHFPF significantly attenuated the ethanol-induced decrease in GES-1 cell survival (82.39 ± 1.93 and 80.10 ± 1.08% vs 56.58 ± 1.86%), inhibited GES-1 cell apoptosis, and alleviated the ethanol-induced gastric mucosal injury (64.76 ± 3.98 and 49.29 ± 3.25%), ulcer index (3.33 ± 0.47 and 4.67 ± 0.47 vs 6.67 ± 0.47), and histopathological changes in mice. Peptide treatment inhibited the phosphorylation and nuclear translocation of nuclear factor kappa B (NF-κB), the secretion of tumor necrosis factor-α, interleukin-6, and endothelin-1. In addition, T. matsutake peptide pretreatment increased growth factor secretion, upregulated B-cell lymphoma-2, downregulated Bcl-2-associated X (Bax), and cleaved cysteinyl aspartate specific proteinase 3, thereby promoting gastric cell survival. These findings strongly suggest that T. matsutake peptides attenuate ethanol-induced inflammatory responses and apoptosis by suppressing NF-κB signaling activation, thereby enhancing gastric epithelial barrier functions.

Tricholoma matsutake-derived peptide WFNNAGP protects against DSS-induced colitis by ameliorating oxidative stress and intestinal barrier dysfunction.

Inflammatory bowel disease (IBD) is a non-specific, chronic inflammatory disease of the intestine. The precise etiology and mechanism underlying the pathogenesis of IBD have not been elucidated. In this study, we investigated the mechanisms through which the Tricholoma matsutake-derived peptide, WFNNAGP, exerts protective effects on the inflammatory response and oxidative stress in a dextran sodium sulfate (DSS)-induced IBD mouse model. WFNNAGP significantly attenuated colitis symptoms in mice, including weight loss, diarrhea, shortened colon, bloody stools, and histopathological changes. WFNNAGP significantly ameliorated the DSS-induced oxidative damage, showing scavenging activity against hydroxyl and DPPH radicals (23.67 ± 4.11% and 34.53 ± 2.45%), increased SOD activity (191.48 ± 4.35 U per mg prot), and decreased MDA activity (1.61 ± 0.24 nmol per mg prot). In addition, WFNNAGP improved the inflammatory response by inhibiting MPO and pro-inflammatory cytokine expression and protected the barrier function by promoting the expression of occludin and ZO-1 in the colon. Western blotting showed that WFNNAGP reduced the inflammatory response by downregulating NF-κB expression and inhibiting the formation and activation of NLRP3 and caspase-1. Thus, WFNNAGP may reduce colonic inflammation in mice by enhancing oxidative defense systems and barrier function and may be a promising candidate for IBD intervention.