[Effect of epigallocatechingallate on acute lung injury induced by oleic acid in mice]

Yao Xue Xue Bao. 2005 Mar;40(3):231-5.
[Article in Chinese]

Abstract

Aim: To investigate the effect of epigallocatechingallate (EGCG) on acute lung injury induced by oleic acid in mice and the possible mechanism.

Methods: Acute lung injury was induced by oleic acid in mice. Light microscopy and electron microscopy were used to examine histological changes and lung index as well as wet to dry weight ratio was calculated. Serum TNF-a level was measured by enzyme linked immunosorbent assay (ELISA) and the phosphorylation of p38 MAPK was determined by Western blotting.

Results: Pretreatment of EGCG significantly alleviated oleic acid induced lung injury accompanied by reduction of lung index and wet to dry weight ratio, decreased of TNF-a level in serum and inhibition of phosphorylation of p38 MAPK.

Conclusion: EGCG showed beneficial effect on acute lung injury induced by oleic acid in mice. The ultimate reduction of TNF-alpha in serum caused by inhibition of phosphorylated p38 MAPK is involved in the mechanism of action of EGCG.

MeSH terms

  • Animals
  • Catechin / analogs & derivatives*
  • Catechin / pharmacology
  • Lung / pathology*
  • Lung / ultrastructure
  • Male
  • Mice
  • Oleic Acid
  • Phosphorylation / drug effects
  • Protective Agents / pharmacology
  • Respiratory Distress Syndrome* / chemically induced
  • Respiratory Distress Syndrome* / metabolism
  • Respiratory Distress Syndrome* / pathology
  • Tumor Necrosis Factor-alpha / metabolism*
  • p38 Mitogen-Activated Protein Kinases / metabolism*

Substances

  • Protective Agents
  • Tumor Necrosis Factor-alpha
  • Oleic Acid
  • Catechin
  • epigallocatechin gallate
  • p38 Mitogen-Activated Protein Kinases