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肖特在癫痫大鼠模型中的抗癫痫作用:代谢轴和肠道微生物群的调节

Antiepileptic Effects of Schott in a Rat Model of Epilepsy: Regulation of Metabolic Axes and Gut Microbiota.

作者信息

Chen Liang, Li Jiaxin, Zhang Wenhui, Wang Jiepeng

机构信息

School of Pharmacy, Guizhou University of Traditional Chinese Medicine, Guiyang 550025, China.

School of Basic Medical Sciences, Hebei University of Chinese Medicine, Shijiazhuang 050200, China.

出版信息

Biology (Basel). 2025 Apr 29;14(5):488. doi: 10.3390/biology14050488.

DOI:10.3390/biology14050488
PMID:40427677
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12108817/
Abstract

As a phytotherapeutic agent with historical applications in epilepsy management, Schott (ATS) remains pharmacologically enigmatic, particularly regarding its pathophysiological mechanisms. This knowledge gap significantly hinders the clinical application of ATS-based treatments. To explore the potential of ATS in combating epileptogenesis, we utilized a pentylenetetrazole (PTZ)-induced chronic epilepsy rat model. Brain metabolomic analysis was performed by ultra-performance liquid chromatography coupled with mass spectrometry (UPLC/MS). Principal component analysis (PCA) and orthogonal projections to latent structures-discriminant analysis (OPLS-DA) were performed for screening differential metabolites. Gut microbiota composition was analyzed through 16S rRNA gene sequencing and examined using Spearman correlation analysis. The results show that oral ATS (50 mg/kg) significantly improved the seizure latency and pathology of rats with epilepsy. Ascorbate and aldarate metabolism, glycerophospholipid metabolism, arachidonic acid metabolism, and intestinal flora were crucial for ATS's ability to counteract epilepsy. The therapeutic effects of ATS against epilepsy were investigated with brain metabolomics and gut microbiota analysis, providing the basis for further comprehensive research.

摘要

作为一种在癫痫治疗中有历史应用的植物治疗剂,肖特(ATS)在药理学上仍然神秘莫测,尤其是在其病理生理机制方面。这一知识空白严重阻碍了基于ATS的治疗方法的临床应用。为了探索ATS在对抗癫痫发生中的潜力,我们使用了戊四氮(PTZ)诱导的慢性癫痫大鼠模型。通过超高效液相色谱-质谱联用(UPLC/MS)进行脑代谢组学分析。进行主成分分析(PCA)和正交投影到潜在结构判别分析(OPLS-DA)以筛选差异代谢物。通过16S rRNA基因测序分析肠道微生物群组成,并使用Spearman相关性分析进行检查。结果表明,口服ATS(50mg/kg)显著改善了癫痫大鼠的癫痫发作潜伏期和病理学。抗坏血酸和醛糖代谢、甘油磷脂代谢、花生四烯酸代谢和肠道菌群对ATS对抗癫痫的能力至关重要。通过脑代谢组学和肠道微生物群分析研究了ATS对癫痫的治疗作用,为进一步的综合研究提供了依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/448a/12108817/06ffb314fb14/biology-14-00488-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/448a/12108817/b4526f5cc964/biology-14-00488-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/448a/12108817/5b960b18249d/biology-14-00488-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/448a/12108817/2a624e205605/biology-14-00488-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/448a/12108817/ba2f89279f84/biology-14-00488-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/448a/12108817/06ffb314fb14/biology-14-00488-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/448a/12108817/b4526f5cc964/biology-14-00488-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/448a/12108817/5b960b18249d/biology-14-00488-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/448a/12108817/2a624e205605/biology-14-00488-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/448a/12108817/ba2f89279f84/biology-14-00488-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/448a/12108817/06ffb314fb14/biology-14-00488-g005.jpg

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本文引用的文献

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Hepatotoxicity Induced by Methyl Eugenol: Insights from Toxicokinetics, Metabolomics, and Gut Microbiota.甲基丁香酚诱导的肝毒性:来自毒代动力学、代谢组学和肠道微生物群的见解
Curr Issues Mol Biol. 2024 Oct 11;46(10):11314-11325. doi: 10.3390/cimb46100673.
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New Value of / Leaves as a Dietary Source for Dementia Prevention.
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Nutrients. 2024 May 23;16(11):1589. doi: 10.3390/nu16111589.
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Butyrate as a potential therapeutic agent for neurodegenerative disorders.丁酸盐作为神经退行性疾病的潜在治疗药物。
Neurochem Int. 2024 Jun;176:105745. doi: 10.1016/j.neuint.2024.105745. Epub 2024 Apr 18.
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Understanding the molecular mechanisms of Acori Tatarinowii Rhizoma: Nardostahyos Radix et Rhizoma in epilepsy treatment using network pharmacology and molecular docking.运用网络药理学和分子对接技术研究石菖蒲-远志治疗癫痫的分子机制
Medicine (Baltimore). 2024 Feb 9;103(6):e37224. doi: 10.1097/MD.0000000000037224.
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