Effects of dexamethasone and ibuprofen on LPS-induced gene expression of TNF alpha, IL-1 beta, and MIP-1 alpha in rat lung

Zhongguo Yao Li Xue Bao. 1997 Mar;18(2):165-8.

Abstract

Aim: To study the kinetics of tumor necrosis factor alpha (TNF alpha), interleukine-1 (IL-1 beta), and macrophage inflammatory protein-1 alpha (MIP-1 alpha) gene expression in rat lung after i.p. lipopolysaccharides (LPS) and the effect of dexamethasone (Dex) and ibuprofen (Ibu) on the cytokines gene expression.

Methods: The amount of Evans blue in lung was measured by fluorescence method. The mRNA levels of TNF alpha, IL-1 beta, and MIP-1 alpha in rat lung were assessed by slot blot analysis.

Results: The mRNA levels of TNF alpha, IL-1 beta, and MIP-1 alpha in rat lung after i.p. LPS increased in a dose-dependent manner, and peaked at 2, 6, and 12 h, respectively. Both Dex 50 mg.kg-1 and Ibu 90 mg.kg-1 injected at 1 h before i.p. LPS markedly decreased the content of Evans blue in lung at 1 h after i.p. LPS. After Dex or Ibu pretreatment, the peak levels of TNF alpha, IL-1 beta, and MIP-1 alpha mRNA decreased markedly compared with LPS alone.

Conclusion: The gene expression of TNF alpha, IL-1 beta, and MIP-1 alpha in rat lung increased after i.p. LPS. Dex and Ibu prevented LPS-induced lung injury through inhibiting the cytokines gene expression.

MeSH terms

  • Animals
  • Anti-Inflammatory Agents / pharmacology
  • Chemokine CCL4
  • Dexamethasone / pharmacology*
  • Gene Expression
  • Ibuprofen / pharmacology*
  • Interleukin-1 / biosynthesis*
  • Lipopolysaccharides / pharmacology
  • Lung / metabolism
  • Macrophage Inflammatory Proteins / biosynthesis*
  • RNA, Messenger / genetics
  • Rats
  • Rats, Wistar
  • Tumor Necrosis Factor-alpha / biosynthesis*

Substances

  • Anti-Inflammatory Agents
  • Chemokine CCL4
  • Interleukin-1
  • Lipopolysaccharides
  • Macrophage Inflammatory Proteins
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha
  • Dexamethasone
  • Ibuprofen