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发酵硅酸杆菌ZS09通过调节脑肠功能改善抗生素诱导的小鼠运动功能障碍
Authors Yang Y, Zhao Y, Lei H, Tan X
Received 19 August 2024
Accepted for publication 19 November 2024
Published 30 November 2024 Volume 2024:17 Pages 10093—10106
DOI https://doi.org/10.2147/JIR.S486018
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Professor Ning Quan
Yang Yang,1 Yuanji Zhao,2 Huan Lei,1 Xiaohong Tan3
1College of Physical Education, Chengdu Sport University, Chengdu, Sichuan, 610041, People’s Republic of China; 2School of Physical Education, Wuhan Sports University, Wuhan, Hubei, 430079, People’s Republic of China; 3Collaborative Innovation Center for Child Nutrition and Health Development, Chongqing University of Education, Chongqing, 400067, People’s Republic of China
Correspondence: Yuanji Zhao, School of Physical Education, Wuhan Sports University, Wuhan, Hubei, 430079, People’s Republic of China, Email 2019029@whsu.edu.cn
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 Limosilactobacillus fermentum 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 Lactobacillus and Bifidobacterium in the gut of mice with motor dysregulation, and decreased the number of Enterococcus and Clostridium perfringens.
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.
Keywords: Limosilactobacillus fermentum, gut function, fatigue, antibiotic, mouse