Dissection of the Functional Mechanism of Human Gut Bacterial Strain AD16 by Secondary Metabolites' Identification, Network Pharmacology, and Experimental Validation.

Dissection of the Functional Mechanism of Human Gut Bacterial Strain AD16 by Secondary Metabolites' Identification, Network Pharmacology, and Experimental Validation.
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通过次级代谢物鉴定、网络药理学和实验验证剖析人肠道细菌菌株 AD16 的功能机制

DOI:
10.3389/fphar.2021.706220
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发表时间:
2021
影响因子:
5.6
通讯作者:
Liu SL
Liu SL
中科院分区:
医学2区
文献类型:
--
作者:
Wang Q;Wang Y;Wang YJ;Ma N;Zhou YJ;Zhuang H;Zhang XH;Li C;Pei YH;Liu SL

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肠道菌属在几种代谢过程中起着重要的作用,例如食欲和食物的摄入量和肠道的苦难,在维持宿主的健康方面也很重要。 。菌株的次生代谢是由生物活性引导的隔离策略,五个新化合物,链球菌A和b(1-2),脊柱杆菌F和G(3-4),以及Eudesmanetetraiol A(5) R和MS分析以及绝对配置通过CD方法确定,网络药理学的分析表明,除了PI3K – AKT信号途径外,AD16的抗NSCLC活性可能是癌症途径的抗NSCLC的关键成分。
Gut microbiota plays important roles in several metabolic processes, such as appetite and food intake and absorption of nutrients from the gut. It is also of great importance in the maintenance of the health of the host. However, much remains unknown about the functional mechanisms of human gut microbiota itself. Here, we report the identification of one anticancer gut bacterial strain AD16, which exhibited potent suppressive effects on a broad range of solid and blood malignancies. The secondary metabolites of the strain were isolated and characterized by a bioactivity-guided isolation strategy. Five new compounds, streptonaphthalenes A and B (1-2), pestaloficins F and G (3-4), and eudesmanetetraiol A (5), together with nine previously known compounds, were isolated from the effective fractions of AD16. Structures of the new compounds were established by 1D and 2D NMR and MS analysis, and the absolute configurations were determined by the CD method. The analysis of network pharmacology suggested that 3, 2, and 13 could be the key components for the anti-NSCLC activity of AD16. In addition to the PI3K–Akt signaling pathway, the proteoglycans in cancer pathway could be involved in the anti-NSCLC action of AD16.
DOI: 10.1021/acs.jafc.0c00878
发表时间: 2020-09-30
影响因子: 6.1
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