Apocynin improves outcome in experimental stroke with a narrow dose range

Neuroscience. 2008 Jun 23;154(2):556-62. doi: 10.1016/j.neuroscience.2008.03.090. Epub 2008 Apr 23.

Abstract

Inflammation following ischemic stroke is known to contribute to injury. NADPH oxidase (NOX) is a major enzyme system originally studied in immune cells that leads to superoxide (O.*) generation. Apocynin is a NOX inhibitor that has been studied as a potential treatment in experimental stroke. Here we explored the effect of different doses of apocynin in a mouse model of 2 h transient middle cerebral artery occlusion (tMCAO) followed by 22 h reperfusion. Apocynin, given i.v. at a dose of 2.5 mg/kg 30 min before reperfusion, improved neurological function (P<0.01), reduced infarct volume (P<0.05), and reduced the incidence of cerebral hemorrhage (P<0.05), but not at higher doses of 3.75 and 5 mg/kg, where it actually increased brain hemorrhage. Apocynin also tended to reduce mortality at the lower dose, but not at higher doses. Using hydroethine fluorescence to delineate O.* in the brain, neurons and some microglia/macrophages, but not vascular endothelial cells were found to contain O.*. Apocynin at protective doses markedly prevented ischemia-induced increases in O.*. Our data suggested that apocynin can protect against experimental stroke, but with a narrow therapeutic window.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetophenones / administration & dosage
  • Acetophenones / pharmacology*
  • Animals
  • Behavior, Animal / drug effects
  • Behavior, Animal / physiology
  • Blood-Brain Barrier / drug effects
  • Blood-Brain Barrier / physiology
  • CD11b Antigen / metabolism
  • Cerebral Infarction / pathology
  • DNA-Binding Proteins
  • Dose-Response Relationship, Drug
  • Enzyme Inhibitors / administration & dosage
  • Enzyme Inhibitors / pharmacology*
  • Intracranial Hemorrhages / complications
  • Intracranial Hemorrhages / drug therapy
  • Intracranial Hemorrhages / pathology
  • Macrophages / metabolism
  • Macrophages / pathology
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Microglia / metabolism
  • Microglia / pathology
  • NADPH Oxidases / antagonists & inhibitors
  • Nerve Tissue Proteins / metabolism
  • Neuroprotective Agents*
  • Nuclear Proteins / metabolism
  • Platelet Endothelial Cell Adhesion Molecule-1 / metabolism
  • Stroke / drug therapy*
  • Stroke / etiology
  • Stroke / pathology
  • Superoxides / metabolism
  • Treatment Outcome

Substances

  • Acetophenones
  • CD11b Antigen
  • DNA-Binding Proteins
  • Enzyme Inhibitors
  • Nerve Tissue Proteins
  • NeuN protein, mouse
  • Neuroprotective Agents
  • Nuclear Proteins
  • Platelet Endothelial Cell Adhesion Molecule-1
  • Superoxides
  • acetovanillone
  • NADPH Oxidases