Astaxanthin Alleviates Dextran Sulfate Sodium-Induced Colitis by Enhancing Intestinal Barrier Integrity and Inflammasome activation 9120

Abstract Description The prevalence of ulcerative colitis (UC) has significantly increased in Asian countries in recent years. This rise, along with the limitations of conventional treatments such as biologics, has spurred interest in alternative remedies for UC management. This study aimed to investigate the protective effects of Astaxanthin (AX) on intestinal integrity and inflammation in a dextran sodium sulfate (DSS)-induced colitis model of inflammatory bowel disease. AX improved transepithelial electrical resistance (TEER) and decreased paracellular permeability in IL-6-stimulated Caco-2 cells by enhancing the expression of tight junction proteins, ZO-1 and occludin. In vivo, AX treatment alleviated DSS-induced colitis symptoms in mice, reducing body weight loss, disease activity index scores, and spleen size, while improving colon length and decreasing serum FITC-dextran levels, indicating enhanced intestinal barrier function. Additionally, AX suppressed NLRP3 inflammasome activation by reducing the levels of pro-caspase-1, cleaved-caspase-1, ASC, and NLRP3 proteins, as well as the mRNA levels of IL-1β, IL-6, and TNF-α. Furthermore, AX treatment restored goblet cell numbers and reduced fibrosis in DSS-induced colitis mice, while also upregulating gene and protein expression of ZO-1 and occludin. In conclusion, AX shows promise as a therapeutic intervention for reducing tissue damage and inflammation in IBD by enhancing intestinal barrier function and inhibiting inflammasome activation. Funding Sources This research was supported by ‘regional innovation mega project ‘ program throught the Korea Innovation Foundation funded by Ministry of Science and ICT (2023-DD-UP-0007) Topic Categories Cellular Adhesion, Migration, and Inflammation (CAM)