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低聚半乳糖合生元通过重塑肠道微生物群和减轻肥大细胞过度活化来缓解肠易激综合征。

and Galacto-Oligosaccharides Synbiotic Relieve Irritable Bowel Syndrome by Reshaping Gut Microbiota and Attenuating Mast Cell Hyperactivation.

作者信息

Yao Qi, Zhang Wenbo, Wang Yuze, Shi Le, Zhao Yixiao, Liang Jiarui, Zhao Yu, Kang Jiawei, Zheng Xudong, Guo Rui, Yuan Tian, She Yongbo, Liu Zhigang

机构信息

Laboratory of Functional Chemistry and Nutrition of Food, College of Food Science and Engineering, Northwest A&F University, Xianyang 712100, China.

Shaanxi Key Laboratory of Natural Products & Chemical Biology, College of Chemistry & Pharmacy, Northwest A&F University, Xianyang 712100, China.

出版信息

Nutrients. 2025 May 14;17(10):1670. doi: 10.3390/nu17101670.

Abstract

BACKGROUND

Irritable bowel syndrome (IBS) significantly impairs the lifestyle and quality of life of the global population. However, the underlying pathophysiological mechanisms remain largely elusive. While conventional pharmacological approaches show limited therapeutic efficacy, emerging microbiota-targeted dietary interventions present promising alternatives.

OBJECTIVES

The present study aimed to elucidate the molecular mechanisms by which a synbiotic mitigates IBS and associated colonic dysfunctions in C57BL/6 mice.

METHODS

The mouse model was induced by a () infection combined with water avoidance stress (WAS). Galacto-oligosaccharides (GOS) were identified as the optimal carbon source for the growth of ZYC501 ( ZYC501), leading to the establishment of the synbiotic formulation.

RESULTS

The 32-day synbiotic intervention, consisting of ZYC501 (1 × 10 CFU/day) and GOS (10 g/L, /), significantly alleviated colonic transit dysfunction, visceral hypersensitivity, and anxiety-like behaviors in IBS mice. The synbiotic treatment significantly inhibited the expression levels of histamine, mast cell tryptase, and prostaglandin E2 (PGE2) ( < 0.05). The synbiotic also suppressed colonic inflammation by reducing the levels of lipopolysaccharide (LPS), , and ( < 0.05). Moreover, the synbiotic increased the expression of MUC2 and the production of short-chain fatty acids (SCFAs), including acetate, propionate, and butyrate ( < 0.05). In terms of gut microbiota modulation, the synbiotic reshaped the gut microbiota composition, increasing the abundance of and while decreasing the levels of and . Correlation analysis further revealed a strong association among SCFAs, colonic inflammation, and the gut microbiota.

CONCLUSIONS

In conclusion, the synbiotic composed of ZYC501 and GOS effectively alleviates IBS and associated colonic dysfunctions by modulating the gut microbiota, reducing mast cell hyperactivity, and enhancing colonic barrier integrity. These findings provide a theoretical basis for developing gut microbiota-targeted dietary interventions for the management of IBS and improvement in gut health.

摘要

背景

肠易激综合征(IBS)严重影响全球人群的生活方式和生活质量。然而,其潜在的病理生理机制仍 largely 难以捉摸。虽然传统的药理学方法显示出有限的治疗效果,但新兴的以微生物群为靶点的饮食干预措施提供了有前景的替代方案。

目的

本研究旨在阐明一种合生元减轻 C57BL/6 小鼠 IBS 及相关结肠功能障碍的分子机制。

方法

小鼠模型通过()感染联合避水应激(WAS)诱导。低聚半乳糖(GOS)被确定为 ZYC501(ZYC501)生长的最佳碳源,从而建立了合生元配方。

结果

由 ZYC501(1×10 CFU/天)和 GOS(10 g/L,/)组成的 32 天合生元干预显著减轻了 IBS 小鼠的结肠转运功能障碍、内脏超敏反应和焦虑样行为。合生元治疗显著抑制了组胺、肥大细胞类胰蛋白酶和前列腺素 E2(PGE2)的表达水平(<0.05)。合生元还通过降低脂多糖(LPS)、、和(<0.05)的水平来抑制结肠炎症。此外,合生元增加了 MUC2 的表达以及短链脂肪酸(SCFAs)的产生,包括乙酸盐、丙酸盐和丁酸盐(<0.05)。在肠道微生物群调节方面,合生元重塑了肠道微生物群组成,增加了和的丰度,同时降低了和的水平。相关性分析进一步揭示了短链脂肪酸、结肠炎症和肠道微生物群之间的强关联。

结论

总之,由 ZYC501 和 GOS 组成的合生元通过调节肠道微生物群、降低肥大细胞过度活性和增强结肠屏障完整性,有效减轻了 IBS 及相关结肠功能障碍。这些发现为开发针对肠道微生物群的饮食干预措施以管理 IBS 和改善肠道健康提供了理论基础。

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