Abstract
Colitis is a colon mucosal disorder characterized by intestinal damage and inflammation. This current study aimed to evaluate the effect of meroterpenoid-rich ethanoic extract of a brown algae, Sargassum macrocarpum (MES) on dextran sulfate sodium (DSS)-induced colitis in mice and explore the possible mechanisms. Mice were given 4% DSS in drinking water for 7 days to induce colitis, followed by 3 days of regular water. MES (12 mg/kg body weight) or celecoxib (10 mg/kg body weight) was administrated orally to mice on a daily basis during these 10 days. Both MES and celecoxib supplementations significantly attenuated DSS-induced weight loss, shortening of colon length, elevated myeloperoxidase activity as well as histomorphological changes of colon. MES and celecoxib reduced the inflammation level of colon tissue, as indicated by its suppression on a panel of pro-inflammatory cytokines, including interleukin (IL)-1β, IL-17, tumor necrosis factor α, and interferon γ, and a group of inflammatory proteins, including intracellular adhesion molecule 1, vascular adhesion molecule 1, matrix metalloproteinase (MMP)-2, MMP-9, MMP-13, and inducible nitric oxidase. In addition, their administration down-regulated pro-inflammatory cytokines in serum. Moreover, the supplementation of MES suppressed the DSS-induced hyperactivation of Akt, JNK, and NF-κB signaling pathways. Taken together, our results demonstrate that MES ameliorates DSS-induced colitis in mice, suggesting that MES may have therapeutic implications for the treatment of colitis.
Highlights
Inflammatory bowel disease (IBD), which includes Crohn’s disease (CD) and ulcerative colitis (UC), is a chronic and recurrent gastrointestinal disorder characterized by recruitment and undesired retention of immune cells in inflamed digestive track
The protective effect of MES against colitis was evaluated by body weight, Disease Activity Index (DAI), and colon length
Colon length shortening is another feature of colitis induced by dextran sulfate sodium (DSS)
Summary
Inflammatory bowel disease (IBD), which includes Crohn’s disease (CD) and ulcerative colitis (UC), is a chronic and recurrent gastrointestinal disorder characterized by recruitment and undesired retention of immune cells in inflamed digestive track. IBD affects millions worldwide and its prevalence increases in Asian countries, such as China and South Korea [3,4,5]. The precise etiology of IBD and underlying mechanisms remain elusive. Therapeutic agents for IBD includes TNF-α antagonists, aminosalicylates, steroids, and immunomodulators [8]. Long-term use of these drugs have adverse effects, such as gastrointestinal intolerance, hepatotoxicity and increased malignancies [9]. Especially with natural origin, for the suppression of IBD are needed
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