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

Yang Yang; Yuanji Zhao; Huan Lei; Xiaohong Tan

doi:10.2147/JIR.S486018

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

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

Authors

Yang Yang¹, Yuanji Zhao², Huan Lei¹, Xiaohong Tan³

Affiliations

¹ College of Physical Education, Chengdu Sport University, Chengdu, Sichuan, 610041, People's Republic of China.
² School of Physical Education, Wuhan Sports University, Wuhan, Hubei, 430079, People's Republic of China.
³ Collaborative Innovation Center for Child Nutrition and Health Development, Chongqing University of Education, Chongqing, 400067, People's Republic of China.

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 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; antibiotic; fatigue; gut function; mouse.

Grants and funding

There is no funding to report.