基於微生物組-代謝組學分析的沒食子酸治療結腸炎研究

原創 藥用植物研究前沿 藥用植物研究前沿 2019-08-12


沒食子酸,一種在水果和蔬菜中發現的植物酚,可減輕潰瘍性結腸炎。然而,沒食子酸治療潰瘍性結腸炎的作用機制尚不清楚。近期,廣州中醫藥大學廖瓊峰研究團隊發表在“Food Funct”名為“A holistic view of gallic acid-induced attenuation in colitis based on microbiome-metabolomics analysis”的論文利用腸道微生物群研究了沒食子酸對潰瘍性結腸炎的治療作用,並利用代謝組學監測了體內代謝的變化,為了解沒食子酸對潰瘍性結腸炎的治療作用提供了一個整體的視角。該研究團隊採用硫酸葡聚糖鈉致大鼠結腸炎模型,連續8天灌胃給與沒食子酸,對糞便樣本進行16S基因測序,獲取細菌群落信息,採用核磁共振法對糞便和尿液樣品進行分析,採用氣相色譜法測定糞便和結腸中短鏈脂肪酸的含量。結果顯示,沒食子酸組潰瘍性結腸炎症狀明顯減輕。硫酸葡聚糖鈉組的微生物變化特徵為益生菌減少,如乳酸菌科和普雷沃式菌科等,部分致病菌增加,主要發生在厚壁菌門和變形桿菌門。給與沒食子酸可使菌群組成恢復到與對照組相似的比例。代謝數據進一步揭示,沒食子酸誘導的代謝變化主要集中在增加葡萄糖相關代謝和膽汁酸代謝,降低氨基酸代謝,這也為微生物群的改變提供了證據,因為這些糞便代謝物是宿主與微生物群相互作用的副產品。這些發現證實了沒食子酸在硫酸葡聚糖鈉致結腸炎中引起了代謝和細菌譜的改變,為了解硫酸葡聚糖鈉治療結腸炎提供了幫助。

基於微生物組-代謝組學分析的沒食子酸治療結腸炎研究

Food Funct 2019;10(7):4046-4061

doi:10.1039/c9fo00213h

A holistic view of gallic acid-induced attenuation in colitis based on microbiome-metabolomics analysis

Gallic acid (GA), a plant phenol found in fruits and vegetables, has been recently reported to attenuate ulcerative colitis (UC). However, the mechanism of GA in UC remains unknown. In this study, we investigated the therapeutic effects of GA on UC from the perspective of gut microbiota and supervised the metabolic alterations in vivo with 1H NMR-based metabolomics, which can provide a holistic view to understand the functions of GA in UC. Rats with dextra sulfate sodium (DSS)-induced colitis were rectally administrated with GA (6 mg kg-1) for 8 consecutive days. 16S gene sequencing was performed on feces samples to obtain bacterial community information. Urine and feces samples were analyzed with 1H NMR spectroscopy, and short chain fatty acids (SCFAs) in feces and colon contents were detected with gas chromatography. Our results showed that UC syndromes in the GA group were significantly attenuated. The microbial alterations in the DSS group were characterized by a decrease of probiotic bacteria, such as Lactobacillaceae and Prevotellaceae, and an increase of some pathogenic species, mainly in the Firmicutes and Proteobacteria phyla. GA treatment could modulate the microbiota composition towards a similar proportion to the control group. Metabolic data further revealed that the GA-induced metabolic changes focus on increasing carbohydrate metabolism (gluco-related metabolism) and bile acid (BA) metabolism and decreasing amino acid metabolism, which also provides evidence for alteration of the microbiota because these feces metabolites are by-products of interactions between the host and the microbiota. These findings demonstrate GA-induced alterations in metabolic and bacterial profiles in DSS-colitis, providing new insight into the attenuation of GA in UC.


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