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神经酸膳食补充通过调节肠道微生物群落-粪便代谢物相互作用改善脑缺血再灌注损伤。

Dietary Supplementation with Nervonic Acid Ameliorates Cerebral Ischemia-Reperfusion Injury by Modulating of Gut Microbiota Composition-Fecal Metabolites Interaction.

机构信息

Key Laboratory of Biotechnology and Resource Utilization of Ministry of Education, Institute of Plant Resources, Dalian Minzu University, Dalian, 116600, China.

School of Pharmaceutical Sciences, Jilin University, Changchun, 130021, China.

出版信息

Mol Nutr Food Res. 2024 Apr;68(8):e2300671. doi: 10.1002/mnfr.202300671. Epub 2024 Apr 2.

Abstract

SCOPE

Cerebral ischemia-reperfusion (IR) injury stands as a prominent global contributor to disability and mortality. Nervonic acid (NA), a bioactive elongated monounsaturated fatty acid, holds pivotal significance in human physiological well-being. This research aims to explore the prophylactic effects and fundamental mechanisms of NA in a rat model of cerebral IR injury.

METHODS AND RESULTS

Through the induction of middle cerebral artery occlusion, this study establishes a rat model of cerebral IR injury and comprehensively assesses the pharmacodynamic impacts of NA pretreatment. This evaluation involves behavioral analyses, histopathological examinations, and quantification of serum markers. Detailed mechanisms of nervonic acid's prophylactic effects are revealed through fecal metabolomics and 16S rRNA sequencing analyses. Our findings robustly support nervonic acid's capacity to ameliorate neurological impairments in rats afflicted with cerebral IR injury. Beyond its neurological benefits, NA demonstrates its potential by rectifying metabolic perturbations across diverse pathways, particularly those pertinent to unsaturated fatty acid metabolism. Additionally, NA emerges as a modulator of gut microbiota composition, notably by selectively enhancing vital genera like Lactobacillus.

CONCLUSION

These comprehensive findings highlight the potential of incorporating NA as a functional component in dietary interventions aimed at targeting cerebral IR injury.

摘要

范围

脑缺血再灌注(IR)损伤是导致残疾和死亡的一个主要全球性问题。神经酸(NA)是一种生物活性的长链单不饱和脂肪酸,对人类生理健康具有重要意义。本研究旨在探讨 NA 在大鼠脑 IR 损伤模型中的预防作用及其基本机制。

方法和结果

通过诱导大脑中动脉闭塞,本研究建立了大鼠脑 IR 损伤模型,并全面评估了 NA 预处理的药效学影响。通过行为分析、组织病理学检查和血清标志物定量评估来进行评价。通过粪便代谢组学和 16S rRNA 测序分析揭示了神经酸预防作用的详细机制。我们的研究结果有力地支持了神经酸改善脑 IR 损伤大鼠神经功能损伤的能力。除了神经学方面的益处外,NA 通过纠正多种途径的代谢紊乱,特别是与不饱和脂肪酸代谢相关的途径,显示出其潜力。此外,NA 作为肠道微生物群落组成的调节剂出现,特别是通过选择性地增强重要属如乳杆菌。

结论

这些综合研究结果强调了将 NA 作为功能性成分纳入旨在针对脑 IR 损伤的饮食干预的潜力。

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