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生物素通过调节大鼠血清素代谢、脑源性神经营养因子、炎症和氧化应激减轻酒精戒断诱导的焦虑和抑郁。

Biotin Mitigates Alcohol Withdrawal-Induced Anxiety and Depression by Regulating Serotonin Metabolism, BDNF, Inflammation, and Oxidative Stress in Rats.

作者信息

Hossaini Dawood, Alipour Adam Khan, Sajjadi Meysam, Ansari Mustafa, Haidary Murtaza

机构信息

Department of Biology and Microbiology, Faculty of Medical Laboratory Technology, Khatam Al-Nabieen University, Kabul, Afghanistan.

Department of Chemistry and Biochemistry, Faculty of Medical Laboratory Technology, Khatam Al-Nabieen University, Kabul, Afghanistan.

出版信息

Neuropsychopharmacol Rep. 2025 Mar;45(1):e12523. doi: 10.1002/npr2.12523.

DOI:10.1002/npr2.12523
PMID:39754400
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11702386/
Abstract

INTRODUCTION

Substance use disorders, particularly alcohol use disorders, represent a significant public health problem, with adolescents particularly vulnerable to their adverse effects. This study examined the possible anxiolytic and antidepressant effects of biotin, a crucial vitamin for brain function, in attenuating the behavioral and neurobiological changes associated with alcohol withdrawal in adolescent rats.

MATERIALS AND METHODS

Sixty male Sprague-Dawley rats were exposed to a 20% ethanol solution for 21 days, followed by a 21-day drug-free period to assess long-term behavioral and physiological changes. Behavioral assessments included the Open Field Test, Elevated Plus Maze, and Forced Swimming Test, administered post-withdrawal to evaluate anxiety and depression behaviors. Additionally, biochemical analyses were performed to measure serotonin levels, monoamine oxidase-A (MAO-A) activity, and BDNF concentrations.

RESULTS

The results indicate that ethanol withdrawal significantly induced anxiety- and depression-like behavior in the rats. However, treatment with biotin, particularly at higher doses, effectively attenuated these withdrawal-related behavioral changes. Mechanistically, biotin administration was found to regulate serotonin levels, monoamine oxidase activity, brain-derived neurotrophic factor, and glial fibrillary acidic protein, and alleviate oxidative stress markers in cortical tissue.

DISCUSSION

The results of this study suggest that biotin may have therapeutic potential for alleviating the negative effects of alcohol withdrawal, particularly those related to anxiety and depression. Further research is needed to elucidate the underlying mechanisms and examine the clinical effects of biotin supplementation for individuals undergoing alcohol withdrawal.

摘要

引言

物质使用障碍,尤其是酒精使用障碍,是一个重大的公共卫生问题,青少年尤其容易受到其不良影响。本研究考察了生物素(一种对脑功能至关重要的维生素)在减轻与青少年大鼠酒精戒断相关的行为和神经生物学变化方面可能具有的抗焦虑和抗抑郁作用。

材料与方法

60只雄性Sprague-Dawley大鼠暴露于20%乙醇溶液中21天,随后进行21天的无药期,以评估长期行为和生理变化。行为评估包括旷场试验、高架十字迷宫试验和强迫游泳试验,在戒断后进行,以评估焦虑和抑郁行为。此外,进行生化分析以测量血清素水平、单胺氧化酶-A(MAO-A)活性和脑源性神经营养因子(BDNF)浓度。

结果

结果表明,乙醇戒断显著诱导大鼠出现焦虑样和抑郁样行为。然而,生物素治疗,尤其是高剂量治疗,有效减轻了这些与戒断相关的行为变化。从机制上讲,发现给予生物素可调节血清素水平、单胺氧化酶活性、脑源性神经营养因子和胶质纤维酸性蛋白,并减轻皮质组织中的氧化应激标志物。

讨论

本研究结果表明,生物素可能具有治疗潜力,可减轻酒精戒断的负面影响,尤其是与焦虑和抑郁相关的影响。需要进一步研究以阐明潜在机制,并考察补充生物素对正在进行酒精戒断的个体的临床效果。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55c5/11702386/d100952d5a78/NPR2-45-e12523-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55c5/11702386/c36fc4a2d399/NPR2-45-e12523-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55c5/11702386/c65b8d56e5b5/NPR2-45-e12523-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55c5/11702386/2fc137ad1dfd/NPR2-45-e12523-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55c5/11702386/2074206ec578/NPR2-45-e12523-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55c5/11702386/c61c826feb57/NPR2-45-e12523-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55c5/11702386/d100952d5a78/NPR2-45-e12523-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55c5/11702386/c36fc4a2d399/NPR2-45-e12523-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55c5/11702386/c65b8d56e5b5/NPR2-45-e12523-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55c5/11702386/2fc137ad1dfd/NPR2-45-e12523-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55c5/11702386/2074206ec578/NPR2-45-e12523-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55c5/11702386/c61c826feb57/NPR2-45-e12523-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55c5/11702386/d100952d5a78/NPR2-45-e12523-g007.jpg

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