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白术内酯I抑制抗生素诱导的肠道微生物群失调。

Atractylenolide I inhibits antibiotic-induced dysbiosis of the intestinal microbiome.

作者信息

Liu Penglin, Zhao Gang, Zhang Lize, Gong Yuxia, Gu Yunfei

机构信息

The First Clinical Medical College of Nanjing University of Chinese Medicine, Nanjing, China.

Department of Proctology, Affiliated Hospital of Qingdao University, Qingdao, China.

出版信息

Ann Transl Med. 2021 Oct;9(20):1539. doi: 10.21037/atm-21-4656.

Abstract

BACKGROUND

Atractylenolide I (AT-I) is an active component that is isolated from Rhizoma Atractylodis macrocephalae and it exerts anti-apoptotic, anti-oxidant, and anti-coagulant properties, and has been widely applied in the treatment of cardiovascular and cerebrovascular diseases in China. This study aimed to investigate the effects and possible mechanism of AT-I on intestinal dysbacteriosis in a mouse model.

METHODS

Mice dysbacteriosis models were established and treated with AT-I, and the intestinal microbiome of the mice were compared. Using antibiotics-induced bacterial elimination in an intestinal dysbacteriosis-associated xenograft model, the gut microbiota-mediated anti-tumor mechanism was investigated.

RESULTS

The intestinal microbiome was changed in the dysbacteriosis mice compared to the control mice, and AT-I could affect the intestinal microbiome of the dysbacteriosis mice. Manipulation of gut bacteria in the intestines of the dysbacteriosis-associated xenograft model further confirmed that the inhibition of tumor progression by AT-I was mediated by the gut microbiota, and that the underlying mechanism involves down-regulation of TLR4/MyD88/NF-κB signaling. AT-I repressed the phosphorylation of p65-NF-κB as well as the downstream cytokines, IL-6 and IL-1β, in dysbacteriosis mice.

CONCLUSIONS

AT-I may inhibit dysbacteriosis by affecting the intestinal microbiome via the regulation of TLR4/MyD88/NF-κB signaling. The present study provides a basis for the application of AT-I as an alternative medication for treating gastrointestinal disorders.

摘要

背景

白术内酯 I(AT-I)是从白术中分离出的一种活性成分,具有抗凋亡、抗氧化和抗凝血特性,在中国已广泛应用于心脑血管疾病的治疗。本研究旨在探讨 AT-I 对小鼠肠道菌群失调的影响及其可能机制。

方法

建立小鼠肠道菌群失调模型并用 AT-I 进行治疗,比较小鼠的肠道微生物群。在肠道菌群失调相关的异种移植模型中使用抗生素诱导细菌清除,研究肠道微生物群介导的抗肿瘤机制。

结果

与对照小鼠相比,肠道菌群失调小鼠的肠道微生物群发生了变化,AT-I 可影响肠道菌群失调小鼠的肠道微生物群。对肠道菌群失调相关异种移植模型小鼠肠道中的细菌进行操控,进一步证实 AT-I 对肿瘤进展的抑制作用是由肠道微生物群介导的,其潜在机制涉及 TLR4/MyD88/NF-κB 信号通路的下调。AT-I 可抑制肠道菌群失调小鼠中 p65-NF-κB 的磷酸化以及下游细胞因子 IL-6 和 IL-1β。

结论

AT-I 可能通过调节 TLR4/MyD88/NF-κB 信号通路影响肠道微生物群来抑制肠道菌群失调。本研究为 AT-I 作为治疗胃肠道疾病的替代药物的应用提供了依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6622/8576645/55a9571dc06c/atm-09-20-1539-f1.jpg

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