Dexamethasone attenuates neutrophil infiltration in the rat kidney in ischemia/reperfusion injury: the possible role of nitroxyl

Free Radic Biol Med. 2001 Sep 15;31(6):809-15. doi: 10.1016/s0891-5849(01)00658-x.

Abstract

Neutrophil infiltration to the tissue, which is one of the important pathogenetic factors in ischemia/reperfusion injury, can be inhibited by glucocorticoids. The purpose of the present study was to clarify the mechanisms by which glucocorticoids inhibit neutrophil infiltration in renal ischemia/reperfusion injury in rats. Pretreatment with dexamethasone significantly attenuated the enhanced neutrophil infiltration and expression of intercellular adhesion molecule-1 induced by renal ischemia/reperfusion. Treatment with nitroxyl anion releaser known as Angeli's salt abolished the beneficial effect of dexamethasone in renal ischemia/reperfusion. Renal dysfunction and tubular damage induced by renal ischemia/reperfusion were not ameliorated by pretreatment with dexamthasone. These results indicate that the attenuation by dexamethasone of neutrophil infiltration and intercellular adhesion molecule-1 expression during renal ischemia/reperfusion may be mediated by the suppressed production of nitroxyl anion. Thus, neutrophil infiltration in renal ischemia/reperfusion injury may be mediated, at least in part, by the enhanced production of nitroxyl anion.

MeSH terms

  • Animals
  • Anions
  • Dexamethasone / pharmacology*
  • Gene Expression / drug effects
  • Glucocorticoids / pharmacology*
  • Intercellular Adhesion Molecule-1 / genetics
  • Kidney / blood supply*
  • Kidney / pathology
  • Male
  • Neutrophils / pathology*
  • Nitrites / pharmacology
  • Nitrogen Oxides / metabolism*
  • Rats
  • Rats, Sprague-Dawley
  • Reperfusion Injury / pathology*

Substances

  • Anions
  • Glucocorticoids
  • Nitrites
  • Nitrogen Oxides
  • Intercellular Adhesion Molecule-1
  • oxyhyponitrite
  • Dexamethasone
  • nitroxyl