SP-8356 inhibits acute lung injury by suppressing inflammatory cytokine production and immune cell infiltration

Int Immunopharmacol. 2024 Apr 20:131:111847. doi: 10.1016/j.intimp.2024.111847. Epub 2024 Mar 21.

Abstract

This study investigated the anti-inflammatory and protective properties of SP-8356, a synthetic derivative of (1S)-(-)-verbenone, in a mouse model of LPS-induced acute lung injury (ALI). By targeting intracellular signaling pathways and inflammatory responses, SP-8356 demonstrated a potent ability to attenuate deleterious effects of proinflammatory stimuli. Specifically, SP-8356 effectively inhibited the activation of crucial signaling molecules such as NF-κB and Akt, and subsequently dampened the expression of inflammatory cytokines in various lung cellular components. Intervention with SP-8356 treatment also preserved the structural integrity of the epithelial and endothelial barriers. By reducing immune cell infiltration into inflamed lung tissue, SP-8356 exerted a broad protective effect against ALI. These findings position SP-8356 as a promising therapeutic candidate for pulmonary inflammatory diseases that cause ALI.

Keywords: Acute lung injury; Inflammatory cytokines; LPS; NF-κB; SP-8356.

MeSH terms

  • Acute Lung Injury* / chemically induced
  • Acute Lung Injury* / drug therapy
  • Acute Lung Injury* / metabolism
  • Animals
  • Bicyclic Monoterpenes*
  • Cytokines / metabolism
  • Lipopolysaccharides / pharmacology
  • Lung
  • Mice
  • NF-kappa B / metabolism
  • Signal Transduction

Substances

  • SP-8356
  • NF-kappa B
  • Cytokines
  • Lipopolysaccharides
  • Bicyclic Monoterpenes