Thalidomide promotes the release of tumor necrosis factor-alpha (TNF-alpha) and lethality by lipopolysaccharide in mice

Biol Pharm Bull. 1998 Jun;21(6):638-40. doi: 10.1248/bpb.21.638.

Abstract

We investigated the in vivo effects of thalidomide on the production of tumor necrosis factor-alpha (TNF-alpha). An in vivo systemic release of TNF-alpha occurred after the injection of lipopolysaccharide (LPS) in male ddY mice, and the TNF-alpha serum levels reached 652.2 +/- 75.7 pg/ml 90 min after the injection of LPS (0.3 mg/kg, i. p.). When thalidomide (1, 3, or 6 mg/kg) was administered intraperitoneally 3 h before the injection of LPS (0.3 mg/kg, i. p.), thalidomide markedly enhanced LPS-induced TNF-alpha release in a dose-dependent manner. The TNF-alpha serum levels at 90 min were 640 +/- 58.6, 1985 +/- 132.6, and 2795 +/- 203.5 pg/ml, respectively, compared to 628.6 +/- 64.4 pg/ml in mice treated with LPS-alone. Pretreatment with a single injection of thalidomide (1, 3, or 6 mg/kg, i. p.) dose-dependently increased the subsequent mortality caused by a challenge with LPS (15 mg/kg, i. p.), a dose that caused death in 10% of the control mice. We conclude that thalidomide enhances in vivo TNF-alpha secretion and the lethality of LPS in mice.

MeSH terms

  • Animals
  • Anti-Inflammatory Agents, Non-Steroidal / toxicity*
  • Dose-Response Relationship, Drug
  • Immunosuppressive Agents / toxicity*
  • Lipopolysaccharides / toxicity*
  • Male
  • Mice
  • Thalidomide / toxicity*
  • Time Factors
  • Tumor Necrosis Factor-alpha / biosynthesis*

Substances

  • Anti-Inflammatory Agents, Non-Steroidal
  • Immunosuppressive Agents
  • Lipopolysaccharides
  • Tumor Necrosis Factor-alpha
  • Thalidomide