Deciphering the mechanism of cimifugin in mitigating LPS-induced neuroinflammation in BV-2 cells

• Zhang Bu ^[1] ; Shan Xu ^[2] ; Feng Xu ^[1]
  1. [1] First Affiliated Hospital of Soochow University

     First Affiliated Hospital of Soochow University

     China

     
  2. [2] Soochow University

     Soochow University

     China

     
• Localización: Allergologia et immunopathologia: International journal for clinical and investigate allergology and clinical immunology, ISSN-e 1578-1267, ISSN 0301-0546, Vol. 52, Nº. 4, 2024, págs. 38-45
• Idioma: inglés
• Texto completo no disponible (Saber más ...)
• Resumen

  • Purpose: Sepsis often triggers a systemic inflammatory response leading to multi-organ dysfunction, with complex and not fully understood pathogenesis. This study investigates the therapeutic effects of cimifugin on BV-2 cells under sepsis-induced stress conditions.

    Methods: We utilized a BV-2 microglial cell model treated with lipopolysaccharide (LPS) to mimic sepsis. Assessments included cellular vitality, inflammatory cytokine quantification (6 interleukin [6IL]-1β, interleukin 6 [IL-6], and tumor necrosis factor-α [TNF-α]) via enzyme-linked-immunosorbent serologic assay, and analysis of mRNA expression using real-time polymerase chain reaction. Oxidative stress and mitochondrial function were also evaluated to understand the cellular effects of cimifugin.

    Results: Cimifugin significantly attenuated LPS-induced inflammatory responses, oxidative stress, and mitochondrial dysfunction. It enhanced cell viability and modulated the secretion and gene expression of inflammatory cytokines IL-1β, IL-6, and TNF-α. Notably, cimifugin activated the deacetylase sirtuin 1–nuclear factor erythroid 2-related factor 2 pathway, contributing to its protective effects against mitochondrial damage.

    Conclusion: Cimifugin demonstrates the potential of being an effective treatment for sepsis--induced neuroinflammation, warranting further investigation.