Modulation of LPS-stimulated pulmonary inflammation by Borneol in murine acute lung injury model

Inflammation. 2014 Aug;37(4):1148-57. doi: 10.1007/s10753-014-9839-8.


The object of our study is to investigate the protective effects of Borneol on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice. To determine the effects of Borneol on the histopathological changes in mice with ALI, inflammatory cell count in bronchoalveolar lavage fluid (BALF) and lung wet/dry weight ratio were measured in LPS-challenged mice, and lung histopathologic changes observed via paraffin section were assessed. Next, cytokine production induced by LPS in BALF and RAW 264.7 cells was measured by enzyme-linked imunosorbent assay (ELISA). To further study the mechanism of Borneol-protective effects on ALI, nuclear factor-kappaB (NF-κB) and mitogen-activated protein kinases (MAPKs) pathways were investigated. In the present study, Borneol obviously alleviated pulmonary inflammation by reducing inflammatory infiltration, histopathological changes, descended cytokine production, and pulmonary edema initiated by LPS. Furthermore, Borneol significantly suppressed phosphorylation of NF-κB/P65, IκBa, p38, JNK, and ERK. Taken together, our results suggest that Borneol suppressed inflammatory responses in LPS-induced acute lung injury through inhibition of the NF-κB and MAPKs signaling pathways. Borneol may be a promising potential preventive agent for acute lung injury treatment.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acute Lung Injury / chemically induced
  • Acute Lung Injury / drug therapy*
  • Animals
  • Bronchoalveolar Lavage Fluid
  • Camphanes / pharmacology*
  • Cell Line
  • Cell Survival
  • Disease Models, Animal
  • Dose-Response Relationship, Drug
  • Interleukin-1beta / metabolism
  • Interleukin-6 / metabolism
  • Lipopolysaccharides / chemistry*
  • Lung / drug effects*
  • MAP Kinase Signaling System
  • Mice
  • NF-kappa B / metabolism
  • Pneumonia / drug therapy*
  • Signal Transduction
  • Tumor Necrosis Factor-alpha / metabolism


  • Camphanes
  • Interleukin-1beta
  • Interleukin-6
  • Lipopolysaccharides
  • NF-kappa B
  • Tumor Necrosis Factor-alpha
  • interleukin-6, mouse
  • isoborneol