Trapa japonica Pericarp Extract Reduces LPS-Induced Inflammation in Macrophages and Acute Lung Injury in Mice

Molecules. 2016 Mar 21;21(3):392. doi: 10.3390/molecules21030392.

Abstract

In this study, we found that chloroform fraction (CF) from TJP ethanolic extract inhibited lipopolysaccharide (LPS)-induced production of nitric oxide (NO) and intracellular ROS in RAW264.7 cells. In addition, expression of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) genes was reduced, as evidenced by western blot. Our results indicate that CF exerts anti-inflammatory effects by down-regulating expression of iNOS and COX-2 genes through inhibition of MAPK (ERK, JNK and p38) and NF-κB signaling. Similarly we also evaluated the effects of CF on LPS-induced acute lung injury. Male Balb/c mice were pretreated with dexamethasone or CF 1 h before intranasal instillation of LPS. Eight hours after LPS administration, the inflammatory cells in the bronchoalveolar lavage fluid (BALF) were determined. The results indicated that CF inhibited LPS-induced TNF-α and IL-6 production in a dose dependent manner. It was also observed that CF attenuated LPS-induced lung histopathologic changes. In conclusion, these data demonstrate that the protective effect of CF on LPS-induced acute lung injury (ALI) in mice might relate to the suppression of excessive inflammatory responses in lung tissue. Thus, it can be suggested that CF might be a potential therapeutic agent for ALI.

Keywords: Trapa japonica pericarp; acute lung injury (ALI); anti-inflammatory effect; bronchoalveolar lavage fluid (BALF).

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acute Lung Injury / chemically induced
  • Acute Lung Injury / drug therapy*
  • Acute Lung Injury / pathology
  • Animals
  • Cyclooxygenase 2 / biosynthesis
  • Gene Expression Regulation / drug effects
  • Humans
  • Inflammation / chemically induced
  • Inflammation / drug therapy*
  • Inflammation / pathology
  • Lipopolysaccharides / toxicity
  • Lythraceae / chemistry
  • Macrophages / drug effects*
  • Macrophages / pathology
  • Male
  • Mice
  • Nitric Oxide / metabolism
  • Nitric Oxide Synthase Type II / biosynthesis
  • Reactive Oxygen Species / metabolism

Substances

  • Lipopolysaccharides
  • Reactive Oxygen Species
  • Nitric Oxide
  • Nitric Oxide Synthase Type II
  • Nos2 protein, mouse
  • Ptgs2 protein, mouse
  • Cyclooxygenase 2