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

被引:11
作者
Guo, Xiangyu [1 ]
Li, Xiangdan [1 ]
Dong, Yanru [1 ]
Xie, Wei [2 ]
Jin, Toufeng [3 ]
Xu, Dongyuan [1 ]
Liu, Lan [4 ]
机构
[1] Yanbian Univ, Key Lab Cellular Funct & Pharmacol Jilin Prov, Yanji 133000, Jilin, Peoples R China
[2] Second Hosp Jilin Univ, Dept Ophthalmol, Changchun, Peoples R China
[3] Yanbian Univ Hosp, Dept Gen Surg, Yanji, Jilin, Peoples R China
[4] Yanbian Univ Hosp, Dept Pathol, Yanji, Jilin, Peoples R China
基金
中国国家自然科学基金;
关键词
Collagen peptide; Fibrosis; Inflammation; Mitogen-activated protein kinase phosphatase-Ulcerative colitis; ACTIVATED PROTEIN-KINASE; ULCERATIVE-COLITIS; PATHOGENESIS; MKP-1; PHOSPHATASE-1; EPIDEMIOLOGY; TRANSITIONS; DYSFUNCTION; MECHANISMS; JNK;
D O I
10.1016/j.jep.2023.116728
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
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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页数:10
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