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宿主-微生物群相互作用:脑缺血急慢性期中的芳香烃受体。

Host-microbiota interactions: The aryl hydrocarbon receptor in the acute and chronic phases of cerebral ischemia.

机构信息

Department of Neurology, Affiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, Hangzhou, China.

Department of Intensive Care Medicine, Affiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, Hangzhou, China.

出版信息

Front Immunol. 2022 Aug 12;13:967300. doi: 10.3389/fimmu.2022.967300. eCollection 2022.

DOI:10.3389/fimmu.2022.967300
PMID:36032153
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9411800/
Abstract

The relationship between gut microbiota and brain function has been studied intensively in recent years, and gut microbiota has been linked to a couple of neurological disorders including stroke. There are multiple studies linking gut microbiota to stroke in the "microbiota-gut-brain" axis. The aryl hydrocarbon receptor (AHR) is an important mediator of acute ischemic damage and can result in subsequent neuroinflammation. AHR can affect these responses by sensing microbiota metabolites especially tryptophan metabolites and is engaged in the regulation of acute ischemic brain injury and chronic neuroinflammation after stroke. As an important regulator in the "microbiota-gut-brain" axis, AHR has the potential to be used as a new therapeutic target for ischemic stroke treatment. In this review, we discuss the research progress on AHR regarding its role in ischemic stroke and prospects to be used as a therapeutic target for ischemic stroke treatment, aiming to provide a potential direction for the development of new treatments for ischemic stroke.

摘要

近年来,肠道微生物群与大脑功能之间的关系受到了广泛的研究,肠道微生物群与包括中风在内的几种神经紊乱有关。有多项研究将肠道微生物群与中风联系起来,构成了“微生物群-肠道-大脑”轴。芳香烃受体 (AHR) 是急性缺血性损伤的重要介质,可导致随后的神经炎症。AHR 可以通过感应微生物群代谢物(特别是色氨酸代谢物)来影响这些反应,并参与调节中风后的急性缺血性脑损伤和慢性神经炎症。作为“微生物群-肠道-大脑”轴的一个重要调节因子,AHR 有可能被用作缺血性中风治疗的新治疗靶点。在这篇综述中,我们讨论了 AHR 在缺血性中风中的作用及其作为缺血性中风治疗的治疗靶点的前景,旨在为缺血性中风的新治疗方法的发展提供一个潜在的方向。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d37/9411800/065392aefa83/fimmu-13-967300-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d37/9411800/e8f0f541dc2c/fimmu-13-967300-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d37/9411800/065392aefa83/fimmu-13-967300-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d37/9411800/e8f0f541dc2c/fimmu-13-967300-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d37/9411800/065392aefa83/fimmu-13-967300-g002.jpg

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本文引用的文献

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Activating AhR alleviates cognitive deficits of Alzheimer's disease model mice by upregulating endogenous Aβ catabolic enzyme Neprilysin.
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