[Effects of dexamethasone on apoptosis and expression of Fas/FasL system in lung tissues of ALI rats]

Zhonghua Jie He He Hu Xi Za Zhi. 2000 Jan;23(1):23-6.
[Article in Chinese]

Abstract

Objective: To determine whether apoptosis occurs in the lung tissues from rats with acute lung injury (ALI), and observe protective effects of dexamethasone by regulating apoptosis of lung tissues in rats with ALI.

Methods: By using TUNEL, in situ hybridization, SqRT-PCR and immunocytochemistry techniques, apoptosis and Fas, FasL expression were studied during early phase of ALI in rats.

Results: LPS leads to the rapid appearance of apoptosis in alveolar epithelial cells and pulmonary vascular endothelial cells at early stage of ALI in rats. The expression of Fas, FasL mRNA and protein was up-regulated in lung tissues of rats with ALI. The administration of dexamethasone suppressed apoptosis as well as expression of Fas, FasL mRNA and protein, inhibited TNF-alpha production and abated lung injury.

Conclusions: The excessive apoptosis and Fas/FasL system may play a role in the pathogenesis of LPS-induced ALI in rats. The protective effects of dexamethasone include inhibiting inflammatory mediators production, suppressing the activation of Fas/FasL system and apoptosis in lung tissues of ALI rats.

MeSH terms

  • Animals
  • Apoptosis / drug effects*
  • Dexamethasone / pharmacology*
  • Fas Ligand Protein
  • Lung / metabolism
  • Lung / pathology*
  • Male
  • Membrane Glycoproteins / analysis
  • Membrane Glycoproteins / genetics*
  • RNA, Messenger / analysis*
  • Rats
  • Rats, Wistar
  • Respiratory Distress Syndrome / drug therapy*
  • Respiratory Distress Syndrome / metabolism
  • Respiratory Distress Syndrome / pathology
  • Tumor Necrosis Factor-alpha / analysis
  • fas Receptor / analysis
  • fas Receptor / genetics*

Substances

  • Fas Ligand Protein
  • Faslg protein, rat
  • Membrane Glycoproteins
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha
  • fas Receptor
  • Dexamethasone