Protective effect of p-cymene on lipopolysaccharide-induced acute lung injury in mice

Inflammation. 2014 Apr;37(2):358-64. doi: 10.1007/s10753-013-9747-3.

Abstract

In the previous study, the anti-inflammatory effect of p-cymene had been found. In this study, we investigated anti-inflammatory effects of p-cymene on acute lung injury using lipopolysaccharide (LPS)-induced acute lung injury (ALI) mouse model. The cell counting in the bronchoalveolar lavage fluid (BALF) was measured. The animal lung edema degree was evaluated by wet/dry weight (W/D) ratio. The superoxidase dismutase (SOD) activity and myeloperoxidase (MPO) activity was assayed by SOD and MPO kits, respectively. The levels of inflammatory mediators including tumor necrosis factor alpha (TNF-α), IL-1β, and IL-6 were assayed by enzyme-linked immunosorbent assay method. The pathological changes of the lung tissues were observed by hematoxylin and eosin staining. The inflammatory signal pathway-related protein levels of NF-κB were measured using Western blotting. The data showed that treatment with the p-cymene markedly attenuated inflammatory cell numbers in the BALF, decreased NF-κB protein level in the lungs, improved SOD activity, and inhibited MPO activity. Histological studies demonstrated that p-cymene substantially inhibited LPS-induced neutrophils in the lung tissue compared with the model group. The results indicated that p-cymene had a protective effect on LPS-induced ALI in mice.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acute Lung Injury / chemically induced
  • Acute Lung Injury / immunology
  • Acute Lung Injury / metabolism
  • Acute Lung Injury / prevention & control*
  • Animals
  • Anti-Inflammatory Agents / pharmacology*
  • Bronchoalveolar Lavage Fluid / immunology
  • Cymenes
  • Cytoprotection
  • Disease Models, Animal
  • Female
  • Inflammation Mediators / metabolism
  • Interleukin-1beta / metabolism
  • Interleukin-6 / metabolism
  • Lipopolysaccharides*
  • Lung / drug effects*
  • Lung / immunology
  • Lung / metabolism
  • Mice
  • Mice, Inbred BALB C
  • Monoterpenes / pharmacology*
  • Neutrophil Infiltration / drug effects
  • Peroxidase / metabolism
  • Pulmonary Edema / chemically induced
  • Pulmonary Edema / prevention & control
  • Superoxide Dismutase / metabolism
  • Transcription Factor RelA / metabolism
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Anti-Inflammatory Agents
  • Cymenes
  • Inflammation Mediators
  • Interleukin-1beta
  • Interleukin-6
  • Lipopolysaccharides
  • Monoterpenes
  • Rela protein, mouse
  • Transcription Factor RelA
  • Tumor Necrosis Factor-alpha
  • interleukin-6, mouse
  • 4-cymene
  • Peroxidase
  • Superoxide Dismutase