Nitric oxide mediates anti-inflammatory action of extracorporeal shock waves

FEBS Lett. 2005 Dec 19;579(30):6839-45. doi: 10.1016/j.febslet.2005.11.023. Epub 2005 Nov 28.

Abstract

Here, we show that extracorporeal shock waves (ESW), at a low energy density value, quickly increase neuronal nitric oxide synthase (nNOS) activity and basal nitric oxide (NO) production in the rat glioma cell line C6. In addition, the treatment of C6 cells with ESW reverts the decrease of nNOS activity and NO production induced by a mixture of lipopolysaccharides (LPS), interferon-gamma (IFN-gamma) plus tumour necrosis factor-alpha (TNF-alpha). Finally, ESW treatment efficiently downregulates NF-kappaB activation and NF-kappaB-dependent gene expression, including inducible NOS and TNF-alpha. The present report suggests a possible molecular mechanism of the anti-inflammatory action of ESW treatment.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anti-Inflammatory Agents / therapeutic use*
  • Cell Line, Tumor
  • Complex Mixtures / pharmacology
  • Electrophoretic Mobility Shift Assay
  • Gene Expression Regulation, Enzymologic / radiation effects*
  • Glioma / chemistry
  • Glioma / drug therapy
  • Glioma / metabolism
  • Glioma / pathology
  • Glioma / therapy
  • High-Energy Shock Waves / therapeutic use*
  • Inflammation / therapy*
  • Interferon-gamma / pharmacology
  • Lipopolysaccharides / pharmacology
  • Microscopy, Confocal
  • Neurons / enzymology
  • Neurons / metabolism
  • Nitric Oxide / antagonists & inhibitors
  • Nitric Oxide / biosynthesis*
  • Nitric Oxide Synthase / analysis
  • Nitric Oxide Synthase / antagonists & inhibitors
  • Nitric Oxide Synthase / metabolism
  • Nitric Oxide Synthase Type II
  • Rats
  • Tumor Necrosis Factor-alpha / pharmacology

Substances

  • Anti-Inflammatory Agents
  • Complex Mixtures
  • Lipopolysaccharides
  • Tumor Necrosis Factor-alpha
  • Nitric Oxide
  • Interferon-gamma
  • Nitric Oxide Synthase
  • Nitric Oxide Synthase Type II