Vanillin protects lipopolysaccharide-induced acute lung injury by inhibiting ERK1/2, p38 and NF-κB pathway

Future Med Chem. 2019 Aug;11(16):2081-2094. doi: 10.4155/fmc-2018-0432.

Abstract

Aim: Thus far, the anti-inflammatory effect of vanillin in acute lung injury (ALI) has not been studied. This study aimed to investigate the effect of vanillin in lipopolysaccharide (LPS)-induced ALI. Results & methodology: Our study detected the anti-inflammatory effects of vanillin by ELISA and western blot, respectively. Pretreatment of mice with vanillin significantly attenuated LPS-stimulated lung histopathological changes, myeloperoxidase activity and expression levels of proinflammatory cytokines by inhibiting the phosphorylation activities of ERK1/2, p38, AKT and NF-κB p65. In addition, vanillin inhibited LPS-induced TNF-α and IL-6 expression in RAW264.7 cells via ERK1/2, p38 and NF-κB signaling. Conclusion: Vanillin can inhibit macrophage activation and lung inflammation, which suggests new insights for clinical treatment of ALI.

Keywords: ALI; inflammatory diseases; lipopolysaccharide; macrophage; vanillin.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acute Lung Injury / drug therapy*
  • Acute Lung Injury / immunology
  • Acute Lung Injury / pathology
  • Animals
  • Anti-Inflammatory Agents / therapeutic use*
  • Benzaldehydes / therapeutic use*
  • Lipopolysaccharides / immunology
  • MAP Kinase Signaling System / drug effects*
  • Male
  • Mice, Inbred BALB C
  • NF-kappa B / antagonists & inhibitors*
  • NF-kappa B / immunology
  • Protein Kinase Inhibitors / therapeutic use

Substances

  • Anti-Inflammatory Agents
  • Benzaldehydes
  • Lipopolysaccharides
  • NF-kappa B
  • Protein Kinase Inhibitors
  • vanillin