Astaxanthin, a xanthophyll carotenoid, prevents development of dextran sulphate sodium-induced murine colitis

• Published in: Journal of Clinical Biochemistry and Nutrition 2019, Vol.64(1), pp.66-72
• Main Authors: Sakai, Shigeki, Nishida, Atsushi, Ohno, Masashi, Inatomi, Osamu, Bamba, Shigeki, Sugimoto, Mitsushige, Kawahara, Masahiro, Andoh, Akira
• Format: Article
• Language: English
• Subjects: Activation; Astaxanthin; Body weight; Body weight loss; c-Jun protein; carotenoid; Carotenoids; Colitis; Colon; Deoxyguanosine; Depletion; Dextran; Dextran sulfate; Drinking water; Epithelial cells; Gene expression; Infiltration; Inflammatory bowel disease; Inflammatory bowel diseases; Interleukin 6; Intestine; Malondialdehyde; MAP kinase; Mice; Mucosa; NF-κB protein; Nuclei (cytology); Oral administration; Original; Plasma levels; Reactive oxygen species; Scavenging; Sodium; Transcription factors; Translocation; Tumor necrosis factor-α; Weight loss; Weight reduction; Xanthophylls
• ISSN: 0912-0009; 1880-5086
• DOI: 10.3164/jcbn.18-47

Astaxanthin is a xanthophyll carotenoid, which possesses strong scavenging effect on reactive oxygen species. In this study, we examined the effect of astaxanthin on dextran sulfate sodium (DSS)-induced colitis in mice. Experimental colitis was induced by the oral administration of 4% w/v DSS in tap water in C57BL/6J mice. Astaxanthin was mixed with a normal rodent diet (0.02 or 0.04%). Astaxanthin significantly ameliorated DSS-induced body weight loss and reduced the disease activity index. The ameliorating effects was observed in a dose-dependent manner. Immunochemical analyses showed that astaxanthin markedly suppressed DSS-induced histological inflammatory changes (inflammatory cell infiltration, edematous changes and goblet cell depletion). Plasma levels of malondialdehyde and 8-hydroxy-2-deoxyguanosine were significantly reduced by the administration of 0.04% astaxanthin. Astaxanthin significantly suppressed the mucosal mRNA expression of IL-1β, IL-6, TNF-α, IL-36α and IL-36γ. Astaxanthin blocked the DSS-induced translocation of NF-κB p65 and AP-1 (c-Jun) into the nucleus of mucosal epithelial cells, and also suppressed DSS-induced mucosal activation of MAPKs (ERK1/2, p38 and JNK). In conclusion, astaxanthin prevented the development of DSS-induced colitis via the direct suppression of NF-κB, AP-1 and MAPK activation. These findings suggest that astaxanthin is a novel candidate as a therapeutic option for the treatment of inflammatory bowel disease.