Lactobacillus brevis is a heterofermentative gram-positive
organism that can be isolated from milk, cheese, sauerkraut, sourdough, silage,
and the mouth and intestinal tract of humans. Lactobacillus brevis CQPC12, a
lactic acid bacterial strain with strong in vitro resistance and potential for
gut colonisation. This study evaluated the neuroprotective and
performance-enhancing effects of Lactobacillus brevis CQPC12 (LBCQPC12),
focusing on its anti-inflammatory and antioxidant properties in a murine model of
systemic perturbation. A state of systemic dysbiosis and inflammation was
induced in mice via intraperitoneal injection of a broad-spectrum antibiotic
cocktail (containing neomycin, vancomycin, amphotericin B, ampicillin, and
metronidazole) combined with lipopolysaccharide. Following intervention with
LBCQPC12, comprehensive assessments were conducted. Functional performance was
evaluated through endurance running and weight-loaded swimming tests.
Histopathological analysis of brain tissue was performed using
hematoxylin-eosin (H&E) staining. Systemic and cerebral oxidative stress
and inflammatory markers were quantified, and gene expression profiles related
to neurotrophic signalling, inflammation, and vascular metabolism in the brain
and skeletal muscle were analysed via quantitative polymerase chain reaction
(qPCR). The results demonstrated that LBCQPC12 treatment significantly improved
physical endurance, as indicated by prolonged running and swimming durations.
It also effectively mitigated systemic and cerebral oxidative stress by
elevating levels of total superoxide dismutase (T-SOD) and glutathione (GSH),
while reducing malondialdehyde (MDA). Concurrently, LBCQPC12 exerted
anti-inflammatory effects, lowering serum and brain concentrations of pro-inflammatory
cytokines interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-α), while
elevating the anti-inflammatory cytokine IL-10, and reducing the liver index.
At the molecular level, LBCQPC12 upregulated key genes in the brain-derived
neurotrophic factor (BDNF) signalling pathway, including protein kinase B 1
(AKT1), cAMP-response element binding protein (CREB), BDNF itself, and
extracellular regulated protein kinases 1 (ERK1). In skeletal muscle, it
enhanced the expression of metabolic and angiogenic factors such as vascular
endothelial growth factor A (VEGF-A), glucose transporter 1 (GLUT-1), GLUT-4,
and hypoxia-inducible factor-1 alpha (HIF-1α). In conclusion, Lactobacillus
brevis CQPC12 demonstrates substantial potential in counteracting antibiotic-induced
central nervous system oxidative inflammation and skeletal muscle impairment,
thereby preserving motor function. These findings position LBCQPC12 as a
promising candidate for the development of next-generation functional probiotic
formulations aimed at supporting neuromotor health.
Author(s) Details
Jiyou Wu
Sports Department, Yunnan Normal University, Kunming 650500, Yunnan, China.
Xiaoguang Yang
College of Physical Education, Yan’an University, Yan’an 716000, Shaanxi,
China.
Yuhua Yang
Department of Sport Management, College of Humanities and
Law, Beijing University of Chemical Technology,
Beijing 100029, China.
Please see the book here :- https://doi.org/10.9734/bpi/mono/978-81-998509-9-6/CH4
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