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ZS09可通过调节脑-肠功能改善抗生素诱导的小鼠运动功能障碍。

ZS09 Can Improve Antibiotic-Induced Motor Dysfunction in Mice by Regulating the Brain-Gut Functions.

作者信息

Yang Yang, Zhao Yuanji, Lei Huan, Tan Xiaohong

机构信息

College of Physical Education, Chengdu Sport University, Chengdu, Sichuan, 610041, People's Republic of China.

School of Physical Education, Wuhan Sports University, Wuhan, Hubei, 430079, People's Republic of China.

出版信息

J Inflamm Res. 2024 Nov 30;17:10093-10106. doi: 10.2147/JIR.S486018. eCollection 2024.

DOI:10.2147/JIR.S486018
PMID:39634287
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11616420/
Abstract

PURPOSE

When consumed in appropriate quantities, probiotics, which are live microorganisms, are good for health. In this study, a mouse model of antibiotic-induced dyskinesia was established using a sterile mixed antibiotic solution to investigate the preventive impact of ZS09 (LFZS09) on this condition in mice.

METHODS

Following modeling, alterations in the serum and brain tissue of mice were assessed for motor measures such as running and swimming, malondialdehyde (MDA), superoxide dismutase, reduced glutathione, interleukin (IL-6, IL-10), and tumor necrosis factor (TNF)-α. The mouse cecum was used to evaluate the relative mRNA expression levels of the intestinal barrier genes, namely occludin-1, zona occludens-1 (ZO-1), and claudin-1. The relative mRNA expression levels of cAMP-response element binding protein (CREB), extracellular signal-regulated kinase (ERK), and brain-derived neurotrophic factor (BDNF) genes in the mouse brain tissue were also evaluated.

RESULTS

Compared with the model group, LFZS09 considerably increased the swimming and running duration of mice, significantly decreased the levels of the inflammatory factors TNF-α and IL-6 and increased SOD expression in the mouse brain, and decreased MDA accumulation in the mouse brain and serum. Furthermore, LFZS09 upregulated occludin-1 gene expression in the cecal tissue to maintain the intestinal barrier, which in turn maintained the normal physiological function of the body. LFZS09 also enhanced the effect of BDNF and increased the expression of BDNF metabolic pathway-related genes, namely CREB, ERK1/2, and BDNF, in the mouse brain tissue. LFZS09 increased the number of and in the gut of mice with motor dysregulation, and decreased the number of and .

CONCLUSION

The findings indicate that LFZS09 regulates antibiotic-induced motor impairment in mice, thereby offering a theoretical foundation for future studies and probiotic or parabiotics production aimed at augmenting motor function.

摘要

目的

益生菌作为活的微生物,适量食用时对健康有益。在本研究中,使用无菌混合抗生素溶液建立抗生素诱导的运动障碍小鼠模型,以研究ZS09(LFZS09)对小鼠这种状况的预防作用。

方法

建模后,评估小鼠血清和脑组织在运动指标(如跑步和游泳)、丙二醛(MDA)、超氧化物歧化酶、还原型谷胱甘肽、白细胞介素(IL - 6、IL - 10)和肿瘤坏死因子(TNF)-α方面的变化。使用小鼠盲肠评估肠道屏障基因(即闭合蛋白 - 1、紧密连接蛋白 - 1(ZO - 1)和克劳丁 - 1)的相对mRNA表达水平。还评估了小鼠脑组织中cAMP反应元件结合蛋白(CREB)、细胞外信号调节激酶(ERK)和脑源性神经营养因子(BDNF)基因的相对mRNA表达水平。

结果

与模型组相比,LFZS09显著增加了小鼠的游泳和跑步持续时间,显著降低了小鼠脑中炎症因子TNF - α和IL - 6的水平,并增加了超氧化物歧化酶的表达,同时减少了小鼠脑和血清中MDA的积累。此外,LFZS09上调盲肠组织中闭合蛋白 - 1基因的表达以维持肠道屏障,进而维持身体的正常生理功能。LFZS09还增强了BDNF的作用,并增加了小鼠脑组织中BDNF代谢途径相关基因(即CREB、ERK1/2和BDNF)的表达。LFZS09增加了运动失调小鼠肠道中[此处原文缺失相关具体内容]的数量,并减少了[此处原文缺失相关具体内容]的数量。

结论

研究结果表明,LFZS09可调节抗生素诱导的小鼠运动功能障碍,从而为未来旨在增强运动功能的研究以及益生菌或合生元生产提供理论基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0227/11616420/d9113e17951f/JIR-17-10093-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0227/11616420/53920eb57917/JIR-17-10093-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0227/11616420/999a434b0b0a/JIR-17-10093-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0227/11616420/88a53ad0a67c/JIR-17-10093-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0227/11616420/86af4b8a1c20/JIR-17-10093-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0227/11616420/aa7d268ad33c/JIR-17-10093-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0227/11616420/d9113e17951f/JIR-17-10093-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0227/11616420/53920eb57917/JIR-17-10093-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0227/11616420/999a434b0b0a/JIR-17-10093-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0227/11616420/88a53ad0a67c/JIR-17-10093-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0227/11616420/86af4b8a1c20/JIR-17-10093-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0227/11616420/aa7d268ad33c/JIR-17-10093-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0227/11616420/d9113e17951f/JIR-17-10093-g0006.jpg

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