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尿石素 A 通过肠道-肌肉轴改善睡眠剥夺引起的运动能力和肠道微生物群。

Urolithin A Ameliorates Athletic Ability and Intestinal Microbiota in Sleep Deprivation from the Perspective of the Gut-Muscle Axis.

机构信息

School of Food Science and Technology, Jiangnan University, Wuxi, 214122, China.

Department of Physical Education, Jiangnan University, Wuxi, 214122, China.

出版信息

Mol Nutr Food Res. 2024 Apr;68(7):e2300599. doi: 10.1002/mnfr.202300599. Epub 2024 Mar 11.

Abstract

SCOPE

Urolithin A (UA), a gut-microbiota-derived metabolite of ellagic acid, presents various benefits to intestinal microecology. The presence of "gut-muscle axis" regulating the onset and progression of exercise-related physical frailty and sarcopenia has been recently hypothesized. This study aims to explore the underlying mechanism of gut-muscle axis by which UA enhances muscle strength and fatigue resistance of sleep-deprived (SD) mice.

METHODS AND RESULTS

UA is gavaged to C57BL/6 mice (50 mg kg bw) before 48-h SD. The results indicate that pretreatment of UA significantly enhances motor ability and energy metabolism. The inflammation is suppressed, and intestinal permeability is improved after prophylactic treatment with UA. The decreased level of serum lipopolysaccharide (LPS) is concomitant with augmentation of the intestinal tight junction proteins. 16s rRNA analysis of colonic contents reveals that UA significantly reduces the abundance of Clostridia_UCG-014 and Candidatus_Saccharimonas, and upregulates Lactobacillus and Muribaculaceae. UA probably influences on gut microbial functions via several energy metabolism pathways, such as carbon metabolism, phosphotransferase system (PTS), and ATP binding cassette (ABC) transporters.

CONCLUSIONS

The dietary intervention of UA helps to create a systemic protection, a bidirectional communication connecting the gut microbiota with muscle system, able to alleviate SD-induced mobility impairment and gut dysbiosis.

摘要

范围

尿石素 A(UA)是鞣花酸的肠道微生物群衍生代谢物,对肠道微生物群具有多种益处。最近假设存在“肠道-肌肉轴”来调节与运动相关的身体虚弱和肌肉减少症的发生和进展。本研究旨在通过 UA 增强睡眠剥夺(SD)小鼠的肌肉力量和抗疲劳能力来探索肠道-肌肉轴的潜在机制。

方法和结果

UA 在 48 小时 SD 之前通过灌胃给予 C57BL/6 小鼠(50mg/kg bw)。结果表明,UA 的预处理可显著增强运动能力和能量代谢。预防性给予 UA 可抑制炎症,改善肠道通透性。血清脂多糖(LPS)水平降低与肠道紧密连接蛋白增加有关。结肠内容物的 16s rRNA 分析表明,UA 可显著降低 Clostridia_UCG-014 和 Candidatus_Saccharimonas 的丰度,并上调乳杆菌和 Muribaculaceae。UA 可能通过几种能量代谢途径(如碳代谢、磷酸转移酶系统(PTS)和 ATP 结合盒(ABC)转运蛋白)影响肠道微生物功能。

结论

UA 的饮食干预有助于创造一种全身性保护,一种连接肠道微生物群与肌肉系统的双向交流,能够缓解 SD 引起的运动障碍和肠道菌群失调。

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