The beta-adrenoceptor agonist clenbuterol is a potent inhibitor of the LPS-induced production of TNF-alpha and IL-6 in vitro and in vivo

Inflamm Res. 1999 Sep;48(9):497-502. doi: 10.1007/s000110050493.


Objective and design: To investigate the suppressive effects of the beta-agonist clenbuterol on the release of TNF-alpha and IL-6 in a lipopolysaccharide (LPS)-model of inflammation, both in vitro and in vivo.

Material and subjects: Human U-937 cell line (monocyte-derived macrophages), and male Wistar rats (200-250 g).

Treatment: U-937 macrophages were incubated with LPS at 1 microg/ml, with or without 1.0 mM-0.1 nM test drugs (clenbuterol and other cAMP elevating agents) for 1-24 h. Rats were administered either 1 or 10 microg/kg clenbuterol (or saline) orally, 1 h before intraperitoneal administration of 2 mg/kg LPS.

Methods and results: TNF-alpha and IL-6 time-concentration profiles were determined both in culture media and plasma, using ELISA' s and bioassays. LPS-mediated release of both cytokines was significantly suppressed by clenbuterol.

Conclusions: The beta-agonist clenbuterol very potently suppresses the LPS-induced release of the pro-inflammatory cytokines TNF-alpha and IL-6 both in vitro and in vivo.

MeSH terms

  • Adrenergic beta-Agonists / pharmacology*
  • Animals
  • Cell Line
  • Clenbuterol / pharmacology*
  • Escherichia coli
  • Humans
  • Interleukin-6 / biosynthesis*
  • Interleukin-6 / metabolism
  • Lipopolysaccharides / pharmacology*
  • Macrophages
  • Male
  • Rats
  • Rats, Wistar
  • Tumor Necrosis Factor-alpha / biosynthesis*
  • Tumor Necrosis Factor-alpha / metabolism


  • Adrenergic beta-Agonists
  • Interleukin-6
  • Lipopolysaccharides
  • Tumor Necrosis Factor-alpha
  • Clenbuterol