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有助于脂多糖喂养的轻度肠道功能障碍小鼠的恢复。

helps in the recovery of lipopolysaccharide-fed mice with mild intestinal dysfunction.

作者信息

Hu Yue, Zhou Jun, Lin Xiaoqi

机构信息

Department of Physiology, Basic Medical College, Shenzhen University, Shenzhen, China.

Shenzhen InnoStar Institute of Biomedical Safety Evaluation and Research Co., Ltd., Shenzhen, China.

出版信息

Front Microbiol. 2025 Mar 12;16:1523742. doi: 10.3389/fmicb.2025.1523742. eCollection 2025.

DOI:10.3389/fmicb.2025.1523742
PMID:40143870
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11938125/
Abstract

BACKGROUND

Mild intestinal dysfunction, linked to subtle yet significant health issues, can be induced by lipopolysaccharide (LPS), a Gram-negative bacterial component that disrupts gut function and triggers inflammation. has shown promise as a probiotic for gut health due to its roles in mucin degradation and short-chain fatty acid production. This study explores the therapeutic effects of on LPS-induced mild intestinal dysfunction in mice.

METHODS

Thirty-eight 6-week-old C57BL/6 mice were split into control ( = 19) and LPS-treated ( = 19) groups. LPS-treated mice received 300 μg/kg/day of LPS for 4 weeks, followed by supplementation at 41 mg/kg/day (Akk1) or 82 mg/kg/day (Akk2) for another 4 weeks. Gut microbiota was analyzed via metagenomic sequencing, and gene expression was evaluated through transcriptomics.

RESULTS

LPS significantly altered gut microbiota, reducing diversity and increasing pathogenic genera like Lachnoclostridium. supplementation, particularly at higher doses, partially restored gut microbiota by increasing beneficial genera such as Muribaculum. Transcriptomics showed that LPS induced immune and inflammatory responses, while reduced these effects by modulating pathways like TNF and NF-kappa B signaling.

CONCLUSION

mitigates LPS-induced gut dysfunction by restoring microbiota balance and modulating immune responses, highlighting its potential as a therapeutic agent for gut health.

摘要

背景

轻度肠道功能障碍与细微但显著的健康问题相关,可由脂多糖(LPS)诱发,脂多糖是一种革兰氏阴性菌成分,会破坏肠道功能并引发炎症。由于其在粘蛋白降解和短链脂肪酸产生中的作用,已显示出作为肠道健康益生菌的潜力。本研究探讨了其对LPS诱导的小鼠轻度肠道功能障碍的治疗作用。

方法

将38只6周龄的C57BL/6小鼠分为对照组(n = 19)和LPS处理组(n = 19)。LPS处理组小鼠接受300μg/kg/天的LPS处理4周,随后分别以41mg/kg/天(Akk1)或82mg/kg/天(Akk2)的剂量补充4周。通过宏基因组测序分析肠道微生物群,并通过转录组学评估基因表达。

结果

LPS显著改变了肠道微生物群,降低了多样性并增加了诸如梭菌属等致病属。补充,尤其是高剂量补充,通过增加诸如穆里杆菌属等有益菌属部分恢复了肠道微生物群。转录组学表明,LPS诱导免疫和炎症反应,而通过调节TNF和NF-κB信号等途径降低了这些影响。

结论

通过恢复微生物群平衡和调节免疫反应减轻了LPS诱导的肠道功能障碍,突出了其作为肠道健康治疗剂的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2696/11938125/758c053014cf/fmicb-16-1523742-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2696/11938125/048b2df022d5/fmicb-16-1523742-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2696/11938125/17749e614259/fmicb-16-1523742-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2696/11938125/cacdc3462c13/fmicb-16-1523742-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2696/11938125/0db4c953909b/fmicb-16-1523742-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2696/11938125/758c053014cf/fmicb-16-1523742-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2696/11938125/048b2df022d5/fmicb-16-1523742-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2696/11938125/17749e614259/fmicb-16-1523742-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2696/11938125/cacdc3462c13/fmicb-16-1523742-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2696/11938125/0db4c953909b/fmicb-16-1523742-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2696/11938125/758c053014cf/fmicb-16-1523742-g005.jpg

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