Title
The β-adrenoceptor agonist clenbuterol is a potent inhibitor of the LPS-induced production of TNF-α and IL-6 in vitro and in vivo
Author
Izeboud, C.A.
Monshouwer, M.
van Miert, A.S.J.P.A.M.
Witkamp, R.F.
Centraal Instituut voor Voedingsonderzoek TNO
Publication year
1999
Abstract
Objective and Design: To investigate the suppressive effects of the β-agonist clenbuterol on the release of TNF-α 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 μg/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 μg/kg clenbuterol (or saline) orally, 1 h before intraperitoneal administration of 2 mg/kg LPS. Methods and Results: TNF-α 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 β-agonist clenbuterol very potently suppresses the LPS-induced release of the pro-inflammatory cytokines TNF-α and IL-6 both in vitro and in vivo.
Subject
Nutrition
β-agonists
Clenbuterol
Cytokines
Lipopolysaccharide
Macrophages
Beta adrenergic receptor stimulating agent
Clenbuterol
Interleukin 6
Lipopolysaccharide
Tumor necrosis factor alpha
Animal cell
Bioassay
Blood level
Controlled study
Culture medium
Cytokine production
Enzyme linked immunosorbent assay
Human
Human cell
Inflammation
Macrophage
Male
Monocyte
Nonhuman
Oral drug administration
Rat
Adrenergic beta-Agonists
Animals
Cell Line
Clenbuterol
Escherichia coli
Humans
Interleukin-6
Lipopolysaccharides
Macrophages
Male
Rats
Rats, Wistar
Tumor Necrosis Factor-alpha
To reference this document use:
http://resolver.tudelft.nl/uuid:be916323-be9b-4491-95c6-b2fbc434467f
DOI
https://doi.org/10.1007/s000110050493
TNO identifier
235186
ISSN
1023-3830
Source
Inflammation Research, 48 (9), 497-502
Document type
article