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Lovastatin dose-dependently potentiates the pro-inflammatory activity of lipopolysaccharide both in vitro and in vivo

ZANIN, VALENTINA
•
MARCUZZI, ANNALISA
•
KLEINER, GIULIO
altro
Zauli, Giorgio
2013
  • journal article

Periodico
JOURNAL OF CARDIOVASCULAR TRANSLATIONAL RESEARCH
Abstract
Since contradictory findings have been reported on potential effects of statins in modulating the inflammatory response, we have analysed the biological activity of lovastatin both in vitro using the Raw 264.7 murine macrophagic cell line and in vivo using BALB/c mice. When added to Raw 264.7 cells in combination with lipopolysaccharide, lovastatin significantly potentiated the release of interleukin-1β, interleukin-6 and interleukin-12 with respect to lipopolysaccharide alone and showed an additive effect on the release of nitric oxide. Similarly, when lovastatin was intraperitoneally administrated to BALB/c mice, it did not induce any pro-inflammatory effect when used alone, but it significantly potentiated the pro-inflammatory activity of lipopolysaccharide, in terms of number of intraperitoneal cells and serum levels of serum amyloid A, interleukin-1β, interleukin-6 and interleukin-12. A potential clinical implication of our study is that lovastatin might exert a pro-inflammatory activity in subjects affected by inflammatory processes, with clinically evident or subclinical infections.
DOI
10.1007/s12265-013-9506-8
WOS
WOS:000327459200010
Archivio
http://hdl.handle.net/11368/2894027
info:eu-repo/semantics/altIdentifier/scopus/2-s2.0-84890561448
Diritti
metadata only access
Soggetti
  • Animal

  • Cell Line

  • Cholesterol

  • Disease Models, Anima...

  • Dose-Response Relatio...

  • Drug Synergism

  • Hydroxymethylglutaryl...

  • Inflammation

  • Inflammation Mediator...

  • Interleukin-12

  • Interleukin-1beta

  • Interleukin-6

  • Macrophage

  • Male

  • Mice

  • Mice, Inbred BALB C

  • Nitric Oxide

  • Serum Amyloid A Prote...

  • Time Factor

  • Lipopolysaccharides

Web of Science© citazioni
12
Data di acquisizione
Mar 21, 2024
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