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在结肠炎小鼠模型中使用低聚果糖、[此处缺失内容]及其组合进行干预。

Intervention with fructooligosaccharides, , and their combination in a colitis mouse model.

作者信息

Wu Yan, Fu Hao, Xu Xu, Jin Hui, Kao Qing-Jun, Teng Wei-Lin, Wang Bing, Zhao Gang, Pi Xiong-E

机构信息

Hangzhou Center for Disease Control and Prevention, Hangzhou, Zhejiang, China.

Institute of Plant Protection and Microbiology, Zhejiang Academy of Agricultural Sciences, Hangzhou, China.

出版信息

Front Microbiol. 2024 May 21;15:1356365. doi: 10.3389/fmicb.2024.1356365. eCollection 2024.

DOI:10.3389/fmicb.2024.1356365
PMID:38835484
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11148295/
Abstract

OBJECTIVE

To examine the effects of an intervention with fructooligosaccharides (FOS), , and their combination in a mouse model of colitis and to explore the mechanisms underlying these effects.

METHODS

The effects of FOS, , and their combination were evaluated in a DSS-induced mouse model of colitis. To this end, parameters such as body weight, the disease activity index (DAI), and colon length were examined in model mice. Subsequently, ELISA was employed to detect the serum levels of proinflammatory cytokines. Histopathological analysis was performed to estimate the progression of inflammation in the colon. Gas chromatography was used to determine the content of short-chain fatty acids (SCFAs) in the feces of model mice. Finally, 16S rRNA sequencing technology was used to analyze the gut microbiota composition.

RESULTS

FOS was slight effective in treating colitis and colitis-induced intestinal dysbiosis in mice. Meanwhile, could significantly reduced the DAI, inhibited the production of IL-1β, and prevented colon shortening. Nevertheless, treatment alone failed to effectively regulate the gut microbiota. In contrast, the combined administration of FOS/ resulted in better anti-inflammatory effects and enabled microbiota regulation. The FOS/ combination (10 CFU/ml and 10 CFU/ml) significantly reduced the DAI, inhibited colitis, lowered IL-1β and TNF-α production, and significantly improved the levels of butyric acid and isobutyric acid. However, FOS/ 10 CFU/ml exerted stronger anti-inflammatory effects, inhibited IL-6 production and attenuated colon shortening. Meanwhile, FOS/ 10 CFU/ml improved microbial regulation and alleviated the colitis-induced decrease in microbial diversity. The combination of FOS and significantly increased the abundance of and decreased the abundance of . Additionally, it promoted the production of acetic acid and propionic acid.

CONCLUSION

Compared with single administration, the combination can significantly increase the abundance of beneficial bacteria such as and and effectively regulate the gut microbiota composition. These results provide a scientific rationale for the prevention and treatment of colitis using a FOS/ combination. They also offer a theoretical basis for the development of nutraceutical preparations containing FOS and .

摘要

目的

研究低聚果糖(FOS)、[此处缺失一种物质名称]及其组合对结肠炎小鼠模型的干预效果,并探讨其作用机制。

方法

在葡聚糖硫酸钠(DSS)诱导的小鼠结肠炎模型中评估FOS、[此处缺失一种物质名称]及其组合的效果。为此,检测模型小鼠的体重、疾病活动指数(DAI)和结肠长度等参数。随后,采用酶联免疫吸附测定(ELISA)法检测促炎细胞因子的血清水平。进行组织病理学分析以评估结肠炎症的进展。利用气相色谱法测定模型小鼠粪便中短链脂肪酸(SCFA)的含量。最后,采用16S核糖体RNA测序技术分析肠道微生物群组成。

结果

FOS对治疗小鼠结肠炎及结肠炎诱导的肠道菌群失调效果轻微。同时,[此处缺失一种物质名称]可显著降低DAI,抑制白细胞介素-1β(IL-1β)的产生,并防止结肠缩短。然而,单独使用[此处缺失一种物质名称]治疗未能有效调节肠道微生物群。相比之下,联合使用FOS/[此处缺失一种物质名称]具有更好的抗炎效果,并能调节微生物群。FOS/[此处缺失一种物质名称]组合(10⁶CFU/ml和10⁷CFU/ml)显著降低DAI,抑制结肠炎,降低IL-1β和肿瘤坏死因子-α(TNF-α)的产生,并显著提高丁酸和异丁酸水平。然而,FOS/10⁶CFU/ml具有更强的抗炎作用,抑制IL-6的产生并减轻结肠缩短。同时,FOS/10⁶CFU/ml改善了微生物调节并缓解了结肠炎诱导的微生物多样性降低。FOS和[此处缺失一种物质名称]的组合显著增加了[某种细菌名称]的丰度并降低了[另一种细菌名称]的丰度。此外,它促进了乙酸和丙酸的产生。

结论

与单一给药相比,联合使用可显著增加有益菌如[某种细菌名称]和[另一种细菌名称]的丰度,并有效调节肠道微生物群组成。这些结果为使用FOS/[此处缺失一种物质名称]组合预防和治疗结肠炎提供了科学依据。它们也为开发含有FOS和[此处缺失一种物质名称]的营养制剂提供了理论基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/993d/11148295/6d89e75da748/fmicb-15-1356365-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/993d/11148295/f3e359681531/fmicb-15-1356365-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/993d/11148295/726c1c9930ae/fmicb-15-1356365-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/993d/11148295/ef84b6a9bbd0/fmicb-15-1356365-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/993d/11148295/8c7e471466fc/fmicb-15-1356365-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/993d/11148295/5cee7b03c9c6/fmicb-15-1356365-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/993d/11148295/71861fb829d4/fmicb-15-1356365-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/993d/11148295/5b8cc2a8d831/fmicb-15-1356365-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/993d/11148295/623df90f3da1/fmicb-15-1356365-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/993d/11148295/6d89e75da748/fmicb-15-1356365-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/993d/11148295/f3e359681531/fmicb-15-1356365-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/993d/11148295/726c1c9930ae/fmicb-15-1356365-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/993d/11148295/ef84b6a9bbd0/fmicb-15-1356365-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/993d/11148295/8c7e471466fc/fmicb-15-1356365-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/993d/11148295/5cee7b03c9c6/fmicb-15-1356365-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/993d/11148295/71861fb829d4/fmicb-15-1356365-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/993d/11148295/5b8cc2a8d831/fmicb-15-1356365-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/993d/11148295/623df90f3da1/fmicb-15-1356365-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/993d/11148295/6d89e75da748/fmicb-15-1356365-g009.jpg

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