Abstract

BackgroundThis study was to investigate the effect and its possible mechanism of fucoidan on the development of spontaneous autoimmune diabetes in non-obese diabetic (NOD) mice.Methods7-week-old NOD mice were randomly divided into three groups: control group, low-dose (300 mg/kg) and high-dose (600 mg/kg) fucoidan-treatment groups. After 5 weeks of treatment, 10 mice per group were randomly selected to be sacrificed after feces collection. The remaining 12 mice per group were fed until 26 weeks of age to assess the incidence of diabetes.ResultsTreatment with fucoidan increased serum insulin level, delayed the onset and decreased the development of diabetes in NOD mice. Fucoidan reduced the levels of strong Th1 proinflammatory cytokines, but induced Th2-bias ed. cytokine response. And dentridic cells (DCs) in fucoidan treatment group were characterized as low expression of MHC class II and CD86 molecules. TLR4 expressions and the downstream molecules in pancreas were down-regulated in fucoidan-treated groups. There were significant differences in the composition of gut flora between NOD control group and fucoidan group. Lactobacillus and Akkermansia were significantly enriched in fucoidan group.ConclusionsFucoidan could prevent the development of autoimmune diabetes in NOD mice via regulating DC/Treg induced immune tolerance, improving gut microecology, down-regulating TLR4 signaling pathway, and maintaining pancreatic internal environment.

Highlights

  • This study was to investigate the effect and its possible mechanism of fucoidan on the development of spontaneous autoimmune diabetes in non-obese diabetic (NOD) mice

  • Effects of fucoidan on glucose tolerance, the incidence of diabetes, serum insulin and LPS levels in NOD mice The glucose tolerance was determined in mice at 12 weeks of age

  • The results showed that the expressions of MHC II and CD86 in CD11c + dendritic cells (DC) in the 12-week-old NOD mice in the fucoidan intervention group was significantly lower than those in the control group

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Summary

Introduction

This study was to investigate the effect and its possible mechanism of fucoidan on the development of spontaneous autoimmune diabetes in non-obese diabetic (NOD) mice. Autoimmune diabetes, known as Type 1 diabetes mellitus (T1DM), is an autoimmune-mediated disease characterized by selective destruction of insulin-producing pancreatic β-cell [1]. The pathogenesis of T1DM relates to genetic factors, autoimmune factors and environmental factors. Based on genetic factors and triggered by environmental factors, it is autoimmune disease. Studies have confirmed that Toll-like receptors (TLRs) are a key family involved in the development of autoimmune inflammation, and inhibition of TLR signaling pathway has great potential in the treatment of autoimmune diseases [2]. The role of TLR4 in T1DM has attracted great attention. Clinical studies have shown that TLR4 expression and ligand levels are

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