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阿拉伯半乳聚糖对 DSS 诱导的慢性结肠炎小鼠模型粪便代谢组的影响。

Impact of arabinogalactan on the fecal metabolome in a DSS-induced chronic colitis mouse model.

机构信息

Collaborative Innovation Center of Seafood Deep Processing, National Engineering Research Center of Seafood, School of Food Science and Technology, Dalian Polytechnic University, Dalian 116034, P. R. China.

National and Local Joint Engineering Laboratory for Marine Bioactive Polysaccharide Development and Application, Dalian Polytechnic University, Dalian 116034, P. R. China.

出版信息

Food Funct. 2022 Aug 15;13(16):8703-8716. doi: 10.1039/d2fo01283a.

DOI:10.1039/d2fo01283a
PMID:35912853
Abstract

Ulcerative colitis (UC) is often accompanied by the dysbiosis of gut microbiota and metabolism. Our previous study indicated that arabinogalactan from (LBP-3) could markedly attenuate the symptoms of chronic UC in mice by modulating the structure of gut microbiota. This study explored the impact of LBP-3 on the fecal metabolomic profiling of the same cohort of mice by HPLC-TripleTOF/MS. Untargeted metabolomic analyses indicated that supplementation with LBP-3 markedly reversed 18 of the 48 differential metabolites (mainly belonging to amino acids and organic acids) disturbed by DSS. Targeted metabolomics revealed that the lower levels of tryptophan, lysine, diiodothyronine, kynurenine, and betaine and higher levels of phenylalanine, leucine, glutamine, isoleucine, homoserine, ()-2-hydroxyglutarate, 2-isopropylmalic acid, ascorbic acid, gluconic acid, and taurine, which were caused by DSS induction, were reversed by LBP-3 treatment. In addition, pathway analysis showed that the pentose phosphate pathway, phenylalanine metabolism, ascorbate and aldarate metabolism, and phenylalanine, tyrosine and tryptophan biosynthesis were strongly affected by LBP-3. More importantly, the above amino acids, organic acids, and metabolic pathways changed by LBP-3 were correlated with the abundance of gut microbiota such as , , , , , , and Ruminococcaceae. This study advances our understanding of the interaction between the microbiome and metabolomics in DSS-induced chronic colitis after LBP-3 treatment.

摘要

溃疡性结肠炎(UC)常伴有肠道微生物群和代谢物的失调。我们之前的研究表明,阿拉伯半乳聚糖(LBP-3)可通过调节肠道微生物群的结构显著减轻慢性 UC 小鼠的症状。本研究通过 HPLC-TripleTOF/MS 探讨了 LBP-3 对同一批小鼠粪便代谢组学图谱的影响。非靶向代谢组学分析表明,LBP-3 补充剂显著逆转了 DSS 扰乱的 48 个差异代谢物中的 18 个(主要属于氨基酸和有机酸)。靶向代谢组学显示,色氨酸、赖氨酸、二碘甲状腺素、犬尿氨酸和甜菜碱水平降低,苯丙氨酸、亮氨酸、谷氨酰胺、异亮氨酸、高丝氨酸、()-2-羟基戊二酸、2-异丙基苹果酸、抗坏血酸、葡萄糖酸和牛磺酸水平升高,这些变化是由 DSS 诱导引起的,LBP-3 处理可逆转这些变化。此外,途径分析表明,LBP-3 强烈影响戊糖磷酸途径、苯丙氨酸代谢、抗坏血酸和醛酸盐代谢以及苯丙氨酸、酪氨酸和色氨酸的生物合成。更重要的是,LBP-3 改变的上述氨基酸、有机酸和代谢途径与肠道微生物群的丰度有关,如、、、、、、和毛螺菌科。本研究加深了我们对 LBP-3 治疗 DSS 诱导的慢性结肠炎后微生物组和代谢组学相互作用的理解。

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