Anti-inflammation effects of fucosylated chondroitin sulphate from Acaudina molpadioides by altering gut microbiota in obese mice
Anti-inflammation effects of fucosylated chondroitin sulphate from Acaudina molpadioides by altering gut microbiota in obese mice
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Acaudina molpadioides 岩藻糖化硫酸软骨素通过改变肥胖小鼠肠道微生物群的抗炎作用
DOI：
10.1039/c8fo02364f
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发表时间：
2019-03-01
期刊：
影响因子：
6.1
通讯作者：
Su, Laijinn
中科院分区：
文献类型：
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作者：
Hu, Shiwei;Wang, Jinhui;Su, Laijinn
这项研究评估了来自海地瓜的膳食岩藻糖基化硫酸软骨素（Am-CHS）对肠道微生物群调节和改善高脂肪饮食喂养小鼠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，包括拟杆菌门减少，厚壁菌门增加，乳杆菌（肠屏障保护剂）和短链脂肪酸（SCFA）产生菌（乳杆菌、双歧杆菌和毛螺菌科NK 4A 136组）增加，以及脂多糖（LPS）产生菌（大肠杆菌）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表达的减少和白细胞介素-10的增加。饮食Am-CHS引起血清和粪便LPS浓度的降低和Toll样受体4（TLR 4）及其下游蛋白的转录抑制。此外，粪便SCFA的门静脉水平增加，这可能导致Am-CHS治疗小鼠中腺苷一磷酸活化蛋白激酶（AMPK）蛋白的增加。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TLR 4信号传导来改善慢性炎症。调节似乎还增加了粪便SCFA的水平，其激活AMPK并最终导致炎症抵抗。
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.