Lobeline improves acute lung injury via nuclear factor-κB-signaling pathway and oxidative stress

Respir Physiol Neurobiol. 2016 May:225:19-30. doi: 10.1016/j.resp.2015.12.003. Epub 2015 Dec 15.

Abstract

Acute lung injury (ALI) is a severe, life-threatening medical condition whose pathogenesis is linked to neutrophil infiltration of the lung. Activation and recruitment of neutrophils to the lung is mostly attributed to the production of chemokines NO, IL-6, for instance. This study aims to investigate lobeline ability in reducing NO production, and nitric oxide synthase (iNOs) expression. Lobeline was tested by inhibiting phosphorylation of mitogen-activated protein kinases (MAPKs), NF-κB and IκBα in LPS-stimulated RAW 264.7 cells. When RAW 264.7 macrophages were given lobeline with LPS, a significant concentration-dependent inhibition of NO production was detected. In vivo tests, mice were either treated with normal saline, 10mg/kg dexmethasone or 5, 10, 20mg/kg lobeline intraperitoneally, and after an hour, the administration of 5mg/kg of LPS was given intratracheally. External performance, cytokines, MAPK pathways and antioxidative enzymes (AOEs) were also carried out to evaluate the effects of these drugs. This is the first investigation in which lobeline was found to effectively inhibit acute lung edema, which may provide a potential target for treating ALI. Lobeline may utilize MAPKs pathways as well as AOEs activity to attenuate LPS-induced nonspecific pulmonary inflammation.

Keywords: ALI; AOEs; IκBα; Lobeline; MAPKs; NF-κB.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acute Lung Injury / drug therapy*
  • Acute Lung Injury / metabolism
  • Animals
  • Cell Line, Tumor
  • Cell Survival / drug effects
  • Cell Survival / physiology
  • Cyclooxygenase 2 / metabolism
  • Dose-Response Relationship, Drug
  • Lipopolysaccharides
  • Lobeline / pharmacology*
  • Macrophages / drug effects
  • Macrophages / physiology
  • Male
  • Mice, Inbred BALB C
  • Mice, Inbred ICR
  • Mitogen-Activated Protein Kinases / metabolism
  • NF-KappaB Inhibitor alpha / metabolism
  • NF-kappa B / metabolism*
  • Nitric Oxide / metabolism
  • Oxidative Stress / drug effects*
  • Oxidative Stress / physiology
  • Random Allocation
  • Signal Transduction / drug effects

Substances

  • Lipopolysaccharides
  • NF-kappa B
  • NF-KappaB Inhibitor alpha
  • Nitric Oxide
  • Lobeline
  • Cyclooxygenase 2
  • Ptgs2 protein, rat
  • Mitogen-Activated Protein Kinases