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• Mannose treatment significantly attenuated DSS-induced intestinal barrier damage. • The AMPK pathway was responsible for the mannose-mediated protective effect in DSS-induced intestinal epithelial damage. • AMPK-AXIN pathway is involved in the mannose-mediated protection of tight junction. Mannose is a unique natural sugar that can be found in a variety of fruits and vegetables. During the past decades, mannose has been reported to be effective in promoting immune tolerance and suppressing inflammatory diseases. Metabolic dysfunction and altered inflammation have clear implications for the development and progression of inflammatory diseases. Herein, we intended to reveal the molecular mechanism of mannose in protecting against intestinal epithelial damage in experimental colitis. We showed that mannose treatment significantly attenuated dextran sodium sulfate (DSS)-induced intestinal barrier damage. The AMPK pathway was responsible for the mannose-mediated protective effect in DSS-induced intestinal epithelial damage. Mechanistically, mannose promoted the axis inhibition protein (AXIN)-based AMPK activation, thereby preventing mitochondrial dysfunction and tight junction disruption in response to the DSS challenge. Cumulatively, the results indicate the use of mannose as a novel approach to treat IBD and other diseases involving tight junction dysfunction. The therapeutic effect of mannose is related to its regulatory function in AMPK pathway activation. [ABSTRACT FROM AUTHOR]

[Display omitted] • Melanin from Sepiapharaonis significantly reduced the depression-anxiety behaviors. • Melanin inhibited NF-κB and NLRP3/ACS/Caspase-1 inflammasome. • Melanin mediated abnormal expression of inflammatory cytokines. • Melanin significantly decreased the activation state of microglia. • Melanin down-regulated oxidative stress levels in the neuroinflammation. The effects of intestinal inflammation on the brain and behavior have received a lot of attention. Melanin (MSI) from Sepiapharaonis ink as an emerging functional food, it exhibited a significant protective effect on dextran sulfate sodium (DSS) induced colitis in previous study. In present study, C57BL/6J mice were free to drink 2.5% DSS solution to establish the colitis model. During the DSS treatment, mice were orally administrated with MSI once per day (75, 150, and 300 mg/kg, respectively). The results showed that MSI treatment ameliorated the depression and anxiety symptoms of colitis mice. Further mechanism studies indicated that MSI alleviated inflammatory response by adjusting cytokines TNF-α, IL-1β, IFN-γ, and IL-10, and proteins NLRP3/ASC/caspase-1 inflammasome), inhibited the activation of microglia, restored brain synaptic density, reduced oxidative stress (SOD, MDA) and regulated apoptosis (tunel staining, caspase-3). MSI could modulate depression-anxiety states by targeting inflammation, nerve tissue, oxidative stress and apoptosis. MSI administration could serve as an emerging blue food and nutrition strategy for the prevention of digestive tract inflammation and behavioral disorders. [ABSTRACT FROM AUTHOR]

[Display omitted] • The effect of melanin from Sepiaesculenta in colitis was studied firstly. • Melanin exhibited superior activity against inflammation and oxidation. • Melanin significantly regulated the intestinal barrier and apoptosis. • Melanin balanced the intestinal flora and metabolism affected by inflammation. Melanin is the major component from Sepiapharaonis ink (MSI), and its anti-inflammatory and antioxidant activities indicate the potential for improvement of inflammatory bowel diseases. The study aimed to investigate how orally-administered MSI on alleviating the dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) and the potential mechanisms. We found that MSI significantly improved DSS-induced weight loss, colon shortening, hematochezia, DAI score, histopathology, and antioxidant indices (SOD and MDA). Further analysis demonstrated that MSI could significantly down-regulate the expression of pro-inflammatory cytokines (TNF-α, IL-1β and IFN-γ) and up-regulate the concentration of anti-inflammatory cytokine IL-10 by regulating TLR4/NF-κB and NLRP3/ASC/Caspase-1 signal pathway. Moreover, tight junction proteins in melanin groups were also maintained by ZO-1 and occludin expressions. In addition, MSI also regulated cellular apoptosis by reducing the expression of pro-apoptosis protein Caspase-3. Interestingly, MSI treatments increased the proportion of dominant bacteria (such as Bacteroidetes and Clostridium) and the abundance of community (alpha diversity, β-diversity, etc.), which significantly balanced microbiota in a dose-dependent manner. In conclusion, oral administration of MSI alleviated DSS-induced colitis by modulating inflammatory cytokines and oxidation stress, maintaining the mucosal barrier, and reverting microbiota changes. [ABSTRACT FROM AUTHOR]

The deficiency of selenium has been found in clinical IBD patients and supplementation selenium is recognized as beneficial for colitis treatment. In this study, an organic selenium compound—selenylation α-D-1,6-glucan (sCPA) was prepared, and the effect of sCPA on DSS induced colitis mice was investigated. The results suggested that sCPA prevented the weight loss, colon length shortening, and stool loose of colitis mice. It protected colon mucosal barrier by promoting tight junction protein ZO-1 and Occludin expression. Moreover, sCPA reduced oxidative stress via regulating SOD and MDA levels, and decreased the contents of inflammatory proteins NF-κB and NLRP3 and adjusted TNF-α, IFN-γ, IL-1β, and IL-10 inflammatory cytokines. Furthermore, sCPA repaired intestinal microbiota composition especially Bacteroidetes, Firmicutes, Proteobacteria, and Actinobacteria that altered by DSS in colitis mice. Meanwhile, SCFAs produced by gut microbiota were restored by sCPA close to the level in the normal group. In conclusion, these findings indicated that the sCPA might be a potential dietary selenium supplementation for the prevention and treatment of colitis. [ABSTRACT FROM AUTHOR]

A homogenous α-D-1,6-glucan (CPA) was extracted from Castanea mollissima Blume. The effect of CPA on ameliorating dextran sulfate sodium induced colitis was investigated. CPA repressed TNF-α and IL-1β level in LPS stimulated RAW264.7 cells. After the intragastric administration of CPA (200 or 400 mg/kg/day), the colon length and body weights of mice with colitis increased and the disease activity index reduced. CPA alleviated colon tissue damage by elevating ZO-1 and occludin protein levels and regulating TNF-α and IL-1β by inhibiting the protein expression of NLPR3 and NF-κB p65. The abundance of Bacteroidetes and Firmicutes was altered and short-chain fatty acid (SCFA) levels, especially propionic, butyric, and isovaleric acids increased significantly. These results indicated that CPA could alleviate colitis by protecting mucosal barriers, reducing inflammation, and regulating intestinal microbiota and SCFA levels. Thus, CPA can be developed as a functional food for the prevention and treatment of colitis. [ABSTRACT FROM AUTHOR]