A Study on the Role of Bifidobacterium Bifidum in Antagonizing Brain Tissue Injury and Inflammation in a Febrile Convulsion Model in Mice

Abstract

Background: Febrile convulsions in children are often triggered by high fever and can lead to acute neurological episodes with potential long-term consequences on cognitive function. Probiotics, particularly bifidobacteria, have demonstrated promising potential in modulating immune function and intestinal health. However, their role in neurological disorders, including febrile convulsions, is yet to be fully explored. Therefore, this study aimed to investigate the therapeutic impacts of Bifidobacterium bifidum on mitigating brain tissue damage and inflammation utilizing a mouse model experiencing febrile convulsions. Methods: To assess the impact of Bifidobacterium bifidum on febrile convulsions, a mouse model was established by administering dry yeast suspension and pentylenetetrazol solution. Using this model, we examined the changes in anal temperature, convulsion onset time, and convulsion duration. Histological analysis through Hematoxylin and Eosin (H&E) staining was employed to study the neuronal morphology in the mouse hippocampus. Furthermore, the levels of serum Cyclic Adenosine Monophosphate (cAMP) and Prostaglandin E2 (PGE₂) were assessed using Enzyme-Linked Immunosorbent Assay (ELISA). Additionally, protein expressions of cyclooxygenase-2 (COX-2), Inducible Nitric Oxide Synthase (iNOS), Gamma-Aminobutyric Acid Type A Receptor (GABAAR), and glial fibrillary acidic protein (GFAP) were determined through western blot analysis, while mRNA expressions of inflammatory markers Interleukin 1 beta (IL-1β), Interleukin 6 (IL-6), and Tumor Necrosis Factor alpha (TNF-α) in hippocampal tissue were determined by quantitative Polymerase Chain Reaction (qPCR). Results: In comparison to the model group, mice in the Bifidobacterium group exhibited a significant reduction in anal temperature (p < 0.05), an increase in the time to onset of convulsions (p < 0.05), a shorter duration of convulsive episodes (p < 0.05), and an enhanced expression of GABAAR protein (p < 0.05). Additionally, the Bifidobacterium group showed lowered serum levels of cAMP and PGE₂ (p < 0.05), improved neuronal cell morphology in the hippocampus, and a decrease in the expression of COX-2, iNOS, and GFAP proteins in the brain tissue (p < 0.05). Furthermore, there was a substantial reduction in the hippocampal tissue levels of pro-inflammatory factors IL-1β, IL-6, and TNF-α mRNA (p < 0.05). Conclusion: Bifidobacterium bifidum exhibits an effective antipyretic and anti-convulsant activity. Its mechanism may be attributed to its ability to reduce fever and inflammation in the brain.