ArticleBMC pharmacology & toxicology2025
Revealing the molecular mechanisms of levofloxacin-induced cognitive impairment and epilepsy: an integrated bioinformatics and molecular dynamics simulation.
Article in BMC pharmacology & toxicology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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Who cites it
4 citing papers in PubMed.
- Bifenthrin exacerbates ulcerative colitis via immunotoxicity: network toxicology and experimental validation reveal novel therapeutic targets.BMC pharmacology & toxicology · 2026Article
- An Updated 16-Year Pharmacovigilance Analysis of Neuropsychiatric Safety Profiles of Ciprofloxacin, Levofloxacin, and Moxifloxacin Using FAERS Data.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Effects of levofloxacin combined with dexamethasone ear drops on suppurative otitis media and analysis of influencing factors.American journal of translational research · 2026Article
- Ginseng-mulberry (medicine-food homologous) pair mitigates cadmium-induced anxiety: a clinical proteomics-guided network pharmacology with rat validation.Frontiers in psychiatry · 2026Article
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Authors and funding
9 authors.
Funding
Abstract
backgroundLevofloxacin is a widely used quinolone antibiotic with good antibacterial properties and high oral utilization. Nevertheless, it is associated with adverse reactions affecting central nervous system (CNS), which in severe cases may include cognitive impairment and epilepsy --potentially life-threatening outcomes. And research on factors contributing to these severe adverse reactions remains limited. Therefore, it is of great significance to investigate the molecular mechanisms underlying levofloxacin-induced CNS injury.
methodsThis study investigated the molecular mechanisms underlying levofloxacin-induced CNS injury by integrating bioinformatics, network toxicology, molecular docking and dynamics simulation. Differentially expressed genes were identified from databases like GEO and Genecards, leading to 33 overlapping drug-disease targets. Subsequently, Protein interaction networks and cytoHubba algorithms identified HSP90AA1 as a key target. Its central role was further validated by receiver operating characteristics (ROC) curves and molecular dynamics simulation. Additionally, GSEA analysis revealed that several pathways that are likely involved.
resultsThis study revealed that levofloxacin may induces CNS injury likely by targeting HSP90AA1 and perturbing key signaling pathways. The key signaling pathways include NOD-like receptor (NLR) signaling pathway, neutrophil extracellular trap (NET) formation, and MAPK signaling pathway. Furthermore, molecular docking revealed a strong binding affinity between levofloxacin and HSP90AA1(-9.9 kcal/mol) and molecular dynamics simulation over 100-ns simulations made further validation.
conclusionThese findings indicate that levofloxacin disrupts neuronal homeostasis via HSP90AA1-mediated inflammatory pathways, providing critical implications for optimizing clinical application of levofloxacin and mitigating its CNS-related risks.
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