Protective effect and mechanism of fucoidan on intestinal mucosal barrier function in NOD mice

Abstract

This study was to evaluate the protective effect of fucoidan on the intestinal mucosal barrier in non-obese diabetic mice (NOD). Twenty NOD mice were randomly assigned to two groups: the control group and the fucoidan intervention group which were fed with fucoidan at a concentration of 600 mg/kg BW (body weight) per day for five weeks. Mice treated with fucoidan had a significant improvement in glycemic control, and the proportions of Th1/Th2/Th17 cells and the levels of endotoxin, DAO and D-LA were reduced. Fucoidan treatment improved intestinal barrier function by increasing ZO-1, claudin-1 and Occludin protein expression. Moreover, the expression levels of phosphorylated ERK1/2, NF-кB p65 and p38 MAPK were decreased. Our result suggested that pre-treatment with fucoidan could attenuate the inflammatory response and maintain intestinal barrier function in NOD mice. Fucoidan-based functional food may be potential for the prevention of T1DM (type 1 diabetes mellitus).

Metabolic regulation mechanism of fucoidan via intestinal microecology in diseases

“…Meanwhile, damage to the intestinal barrier could allow diamine oxidase, d ‐lactic acid and endotoxin to penetrate the internal circulation, a sign of intestinal permeability. This finding was further supported by a study in non‐obese diabetic mice, a model of autoimmune diabetes; after fucoidan intervention (600 mg kg −1 ), the expression of occludin, zonula occludens 1, claudin‐1 was increased, and the levels of diamine oxidase, d ‐lactic acid and endotoxin were reduced 10 …”

“…Our previous research found that fucoidan‐treatment (600 mg kg −1 ) notably reduced the levels of IFN‐γ, IL‐17A and down‐regulated the IFN‐γ/IL‐4 ratio in mice. In other words, fucoidan regulated the equilibrium of Th1/Th2/Th17 10 …”

“…Nuclear factor‐kappa B (NF‐κB) is one of the signaling pathways of inflammation. NF‐κB is released into the nucleus after being activated by inflammatory stimuli (such as lipopolysaccharides) and then transcriptionally induces inflammation‐related genes 10 . Pro‐inflammatory cytokines, such as interferon‐γ (IFN‐γ) and tumor necrosis factor α (TNF‐α) can induce apoptosis of intestinal epithelial cells and affect the expression of TJ proteins, ultimately destroying the function of the intestinal mucosal barrier 11,12 .…”

Aureusidin derivative CNQX inhibits chronic colitis inflammation and mucosal barrier damage by targeting myeloid differentiation 2 protein

“…Meanwhile, TEM can reveal the severe damage of the structure of mouse intestinal villi. 25,26 DSS can induce the activation of TLR4 signal in the mouse intestine. CNQX can significantly alleviate this damage and attenuate he inflammatory response in the mouse intestine.…”

“…DSS can destroy the intestinal mucosa of mice and obviously damage the mucosal barrier of mice, which is manifested as the down‐regulated expression of tight junction protein (occludin and claudin‐1). Meanwhile, TEM can reveal the severe damage of the structure of mouse intestinal villi 25,26 . DSS can induce the activation of TLR4 signal in the mouse intestine.…”