Dietary polysaccharide-rich extract from Eucheuma cottonii modulates the inflammatory response and suppresses colonic injury on dextran sulfate sodium-induced colitis in mice

Abstract

Inflammatory bowel disease (IBD) is a known medical burden in most developed countries and a significant cause of morbidity. The IBD label includes Crohn's disease (CD) and ulcerative colitis (UC). Pharmacological and surgical intervention are the two main management approaches for IBD. Some drugs have been developed for IBD therapy, but accessibility is limited due to high costs. Furthermore, these agents have demonstrated inactivity over long-term treatment courses. Therefore, an urgent need is present for new treatment options that are safe, able to sustain clinical remission, and improve mucosal gut healing. Seaweed has received much attention in the pharmacological field owing to its various biomedical properties, including the prolongation of blood clotting time, as well as antitumor, anti-inflammation, and antioxidant effects. This study therefore aimed to examine the effects of a dietary polysaccharide-rich extract obtained from Eucheuma cottonii (EC) on a model of colitis. Colitis was induced in male BALB/c mice by the administration of 2.5% (w/v) dextran sulfate sodium (DSS) for 7 days. DSS-induced mice were treated with either one of three different doses of EC extracts (0.35, 0.70, and 1.75 g/kg body weight) or curcumin as a positive control (0.10 g/kg). Mice were sacrificed post-treatment and blood samples were collected. The disease activity index (DAI) and inflammatory cytokine levels (tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, IL-10) were measured. After treatment for 7 days, EC extract administration protected against weight loss and decreased the colon weight per length ratio. EC extract administration also decreased pro-inflammatory cytokine expression, increased IL-10 levels, and reduced colonic damage. Therefore, a dietary polysaccharide-rich extract from E. cottonii reduced DSS-induced bowel inflammation, thereby becoming a promising candidate for the treatment of colitis.

Fig 1. Flowchart of dextran sulfate sodium (DSS) induction of colitis in mice.

Fig 2. Cell viability of RAW 264.7 macrophage after treatment with EC extract for 24 h.

Data are shown as the mean ± S.D. (n = 5). Different letters (a-b) indicate statistical significance (P<0.05) as determined by Duncan’s multiple range test.

Fig 3. Effect of EC extract on (a) weight loss and (b) disease activity index in DSS-treated mice during and after 7 days of treatment.

Data are shown as the mean ± S.D. (n = 8). Letters indicate statistical significance (P<0.05) as analyzed by Duncan’s multiple range test.

Fig 4. Effects of EC extract treatment on colon health after 7 days of treatment: (a) colon length, (b) colon weight/length ratio, (c) splenic weight, (d) representative colons for each group.

Data are shown as the mean ± S.D. (n = 8). Letters indicate statistical significance (P<0.05) as analyzed by Duncan’s multiple range test.

Fig 5. Effects of EC extract on inflammatory cytokine expression in serum after 7 days of treatment: (a) TNF-α, (b) IL-6, and (c) IL-1β.

Data are shown as the mean ± S.D. (n = 8). Letters indicate statistical significance (P<0.05) as analyzed by Duncan’s multiple range test.

Fig 6. Effects of EC extract on inflammatory cytokine expression in colon tissue after 7 days of treatment: (a) IL-1β and (b) IL-10.

Data are shown as the mean ± S.D. (n = 8). Letters indicate statistical significance (P<0.05) as analyzed by Duncan’s multiple range test.

Fig 7. Representative colonic tissue histopathology for each group after 7 days of treatment.