Enhancing Effects of Lactobacillus brevis CQPC12 on Motor Function in Mice Damaged by Antibiotics

Abstract

This study aims to investigate the potential anti-inflammatory and antioxidant properties of Lactobacillus brevis CQPC12 (LBCQPC12) to enhance brain, neural, and motor functioning in mice. Mice were given intraperitoneal injections of mixed antibiotics (5 mg/mL neomycin, 25 mg/mL vancomycin, 0.1 mg/mL amphotericin B, 10 mg/mL ampicillin, 5 mg/mL metronidazole, and 1.5 μg/mL lipopolysaccharide) to mimic human bodies. At the conclusion of the trial, the mice’s capacity to run for prolonged periods of time and swim with weight was assessed. Furthermore, hematoxylin–eosin (H&E) staining was employed to investigate pathological alterations in brain tissue; quantitative polymerase chain reaction (qPCR) was applied to discover inflammatory pathway genes and vascular endothelial growth factor (VEGF)-related expressions in the brain and skeletal muscle, and the liver index, serum, and brain oxidation, and inflammation indicators were found. The findings demonstrated that LBCQPC12 increased total superoxide dismutase (T-SOD), glutathione (GSH), and interleukin-10 (IL-10) levels while decreasing malondialdehyde (MDA), IL-6, and tumor necrosis factor alpha (TNF-α) levels in the serum and brain, as well as lengthening the mice’s weight-carrying swimming and running durations and lowering the liver index. LBCQPC12 boosted the expression of VEGF-A, glucose transporter 1 (GLUT-1), GLUT-4, and hypoxia-inducible factor-1 alpha (HIF-1α) mRNA in skeletal muscle as well as genes in the brain’s protein kinase B 1/cAMP-response element binding protein/brain-derived neurotrophic factor/extracellular regulated protein kinases 1 (AKT1/CREB/BDNF/ERK1) pathways. Finally, LBCQPC12 demonstrated potential utility in the creation of functional probiotics by reducing oxidative inflammation, skeletal muscle damage, and motor function in the central nervous system brought on by antibiotics.