Wogonoside alleviates microglia-mediated neuroinflammation via TLR4/MyD88/NF-κB signaling axis after spinal cord injury

Eur J Pharmacol. 2024 Jun 15:973:176566. doi: 10.1016/j.ejphar.2024.176566. Epub 2024 Apr 16.

Abstract

Wogonoside (WG) is a natural flavonoid extracted from Scutellariae Radix, recognized for its established anti-inflammatory properties. However, the role of WG in the context of neuroinflammation after spinal cord injury (SCI) remains inadequately elucidated. This study employed in silico, in vitro, and in vivo methodologies to investigate the impact of WG on microglia-mediated neuroinflammation after SCI. In the in silico experiment, we identified 15 potential target genes of WG associated with SCI. These genes were linked to the regulation of inflammatory response and immune defense. Molecular docking maps revealed toll-like receptor 4 as a molecular target for WG, demonstrating binding through a hydrogen bond (Lys263, Ser120). In lipopolysaccharide-stimulated BV2 cells and SCI mice, WG significantly attenuated microglial activation and facilitated a phenotype shift from M1 to M2. This was evidenced by the reversal of the increased expressions of Iba1, GFAP, and iNOS, as well as the decreased expression of Arg1. WG also suppressed the production of pro-inflammatory mediators (NO, TNF-α, IL-6, IL-1α, IL-1β, C1q). WG exerted these effects by suppressing the TLR4/MyD88/NF-κB signaling axis in microglia. Furthermore, by reducing levels of TNF-α, IL-1α, and C1q in supernatant of LPS-induced microglia, WG indirectly induced astrocytes change to A2 phenotype, evidenced by transcriptome sequencing result of primary mouse astrocytes. All these events above collectively created a favorable microenvironment, contributing to a significant alleviation of weight loss and neuronal damage at the lesion site of SCI mice. Our findings substantiate the efficacy of WG in mitigating neuroinflammation after SCI, thereby warranting further exploration.

Keywords: Astrocyte; Microglia; Neuroinflammation; Spinal cord injury; TLR4/MyD88/NF-κB signaling axis; Wogonoside.

MeSH terms

  • Animals
  • Anti-Inflammatory Agents / pharmacology
  • Anti-Inflammatory Agents / therapeutic use
  • Cell Line
  • Flavanones* / pharmacology
  • Flavanones* / therapeutic use
  • Glucosides* / pharmacology
  • Glucosides* / therapeutic use
  • Inflammation Mediators / metabolism
  • Lipopolysaccharides / pharmacology
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Microglia* / drug effects
  • Microglia* / metabolism
  • Microglia* / pathology
  • Molecular Docking Simulation
  • Myeloid Differentiation Factor 88* / metabolism
  • NF-kappa B* / metabolism
  • Neuroinflammatory Diseases* / drug therapy
  • Neuroinflammatory Diseases* / metabolism
  • Neuroprotective Agents / pharmacology
  • Neuroprotective Agents / therapeutic use
  • Signal Transduction* / drug effects
  • Spinal Cord Injuries* / drug therapy
  • Spinal Cord Injuries* / metabolism
  • Spinal Cord Injuries* / pathology
  • Toll-Like Receptor 4* / metabolism

Substances

  • Toll-Like Receptor 4
  • NF-kappa B
  • Myeloid Differentiation Factor 88
  • Glucosides
  • wogonoside
  • Flavanones
  • Tlr4 protein, mouse
  • Myd88 protein, mouse
  • Lipopolysaccharides
  • Anti-Inflammatory Agents
  • Inflammation Mediators
  • Neuroprotective Agents