4.7 Article

Cod (Gadus) skin collagen peptide powder reduces inflammation, restores mucosal barrier function, and inhibits fibrosis in dextran sodium sulfate-induced colitis in mice

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JOURNAL OF ETHNOPHARMACOLOGY
卷 316, 期 -, 页码 -

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ELSEVIER IRELAND LTD
DOI: 10.1016/j.jep.2023.116728

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Collagen peptide; Fibrosis; Inflammation; Mitogen-activated protein kinase phosphatase-Ulcerative colitis

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This study aimed to investigate the preventive and protective effect of cod skin collagen peptide powder (CP) on mice with ulcerative colitis (UC) and explore the underlying mechanism. The results showed that CP reduced inflammation by upregulating mitogen-activated protein kinase phosphatase-1 (MKP-1) and polarizing macrophages toward the M2 phenotype. It also inhibited the development of fibrosis complicating UC by regulating the expression of ZO-1, Occludin, α-SMA, Vimentin, Snail, and Slug.
Ethnopharmacological relevance: Ulcerative colitis (UC) is a chronic inflammatory bowel disease of unknown etiology. Cod (Gadus), a kind of herb from the Chinese herb. Traditionally, it has used to treat trauma, reduce swelling and relieve pain in order to exert its anti-inflammatory activity. Recent reports based on its hydrolyzed or enzymatic extracts have shown its anti-inflammatory, mucosal barrier protecting properties. However, its mechanism of improvement in ulcerative colitis is not clear. Aim of the study: This study aimed to explore the preventive and protective effect of cod skin collagen peptide powder (CP) on mice with UC and to explore the underlying mechanism. Materials and methods: Mice with dextran sodium sulfate (DSS)-induced UC were treated with CP by gavage, and the anti-inflammatory effects of CP were assessed using general physical, pro-inflammatory cytokine, histo-pathological, immunohistochemical, macrophage flow cytometry, and inflammatory signaling pathway assays. Results: CP ameliorates inflammation by upregulating mitogen-activated protein kinase phosphatase-1 (MKP-1) and thereby decreasing the phosphorylation levels of P38 and JNK. It also polarizes macrophages in the colon towards the M2 phenotype, which helps to reduce tissue damage and promotes colon repair. At the same time, CP also inhibits the development of fibrosis, one of the complications of UC, by upregulating ZO-1, Occludin, and downregulating & alpha;-SMA, Vimentin, Snail, and Slug. Conclusion: In this study, we found CP reduced inflammation in mice with UC by inducing MKP-1 expression, which caused dephosphorylation of mitogen-activated protein kinase (MAPK). CP also restored mucosal barrier function and inhibited the development of fibrosis complicating UC in these mice. Taken together, these results suggested that CP improved the pathological manifestations of UC in mice, suggesting that it can play a bio-logical role as a nutritional supplement for preventing and treating UC.

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