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海洋生物多糖硫酸软骨素通过改变肥胖小鼠肠道微生物群发挥抗炎作用。

Anti-inflammation effects of fucosylated chondroitin sulphate from Acaudina molpadioides by altering gut microbiota in obese mice.

机构信息

Innovation Application Institute, Zhejiang Ocean University, Zhoushan, Zhoushan, 316022, China.

出版信息

Food Funct. 2019 Mar 20;10(3):1736-1746. doi: 10.1039/c8fo02364f.

DOI:10.1039/c8fo02364f
PMID:30855043
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.

摘要

本研究评估了来自棘尾虫(Acaudina molpadioides)的膳食岩藻糖基硫酸软骨素(Am-CHS)对高脂肪饮食喂养的小鼠肠道微生物群的调节和改善慢性炎症风险因素的可能益生元作用。结果表明,Am-CHS 处理极大地改变了肠道微生物群,包括厚壁菌门(Bacteroidetes)的减少、拟杆菌门(Firmicutes)的增加、乳杆菌(肠道屏障保护者)和短链脂肪酸(SCFA)产生菌(乳杆菌、双歧杆菌和lachnospiraceae NK4A136 组)的增加,以及内毒素(LPS)产生菌(大肠杆菌)的减少。这种调节抑制了炎症反应,表现为循环促炎细胞因子及其 mRNA 表达的减少,以及白细胞介素-10 的增加。膳食 Am-CHS 导致血清和粪便 LPS 浓度降低,并抑制 Toll 样受体 4(TLR4)及其下游蛋白的转录。此外,门脉水平的粪便 SCFAs 增加,这可能导致 Am-CHS 处理的小鼠中腺苷单磷酸激活蛋白激酶(AMPK)蛋白增加。这些结果表明,Am-CHS 对肠道微生物群的调节可以通过降低 LPS 水平和 TLR4 信号来改善慢性炎症。调节似乎也增加了粪便 SCFAs 的水平,激活 AMPK,最终导致炎症抵抗。

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