Anti-inflammation effects of fucosylated chondroitin sulphate from Acaudina molpadioides by altering gut microbiota in obese mice. Issue 3 (11th March 2019)

• Record Type: Journal Article
• Authors: Hu, Shiwei; Wang, Jinhui; Xu, Yangli; Yang, Huicheng; Wang, Jingfeng; Xue, Changhu; Yan, Xiaojun; Su, Laijinn
• Is Part Of: Food & function. Volume 10:Issue 3(2019)
• Page Start: 1736
• Page End: 1746
• Publication Date: 2019-03-11
• Subjects: Food -- Analysis -- Periodicals; Food -- Composition -- Periodicals; Nutrition -- Periodicals; 664.07
• DOI: 10.1039/c8fo02364f
• Languages: English
• ISSNs: 2042-6496

Abstract

Abstract : Fucosylated chondroitin sulfate from Acaudina molpadioides ( Am -CHS) can improve chronic inflammation through modulation of gut microbiota via inhibition of LPS/TLR4 signaling and activation of the SCFAs/AMPK pathway. Abstract : This study evaluated the possible prebiotic effects of dietary fucosylated chondroitin sulfate from Acaudina molpadioides ( Am -CHS) on the modulation of the gut microbiota and the improvement in the risk factors for chronic inflammation in high fat diet-fed mice. The results showed that the Am -CHS treatment greatly modified the gut microbiota, including the decrease in Bacteroidetes, increase in Firmicutes, elevation in Lactobacillus (intestinal barrier protector) and short chain fatty acid (SCFA)-producing bacteria ( Lactobacillus, Bifidobacterium, and Lachnospiraceae NK4A136 group ), and reduction in the lipopolysaccharide (LPS) producer ( Escherichia coli ). This modulation inhibited inflammatory response, manifesting the decreases in circulating proinflammatory cytokines and their mRNA expression, and the increases in interleukin-10. Dietary Am -CHS caused reductions in serum and fecal LPS concentrations and inhibition of transcription of toll-like receptor 4 (TLR4) and its downstream proteins. In addition, there were increases in the portal levels of fecal SCFAs, which probably contributed to an increase in the adenosine monophosphate-activated protein kinase (AMPK) protein in Am -CHS-treated mice. These results suggest that modulation of gut microbiota by Am -CHS can improve chronic inflammation by reducing LPS levels and TLR4 signaling. Modulation also appears to increase the levels of fecal SCFAs, which activates AMPK and finally leads to inflammation resistance.