Metallic gold reduces TNFalpha expression, oxidative DNA damage and pro-apoptotic signals after experimental brain injury

Brain Res. 2009 May 19:1271:103-13. doi: 10.1016/j.brainres.2009.03.022. Epub 2009 Mar 25.

Abstract

Brain injury represents a major health problem and may result in chronic inflammation and neurodegeneration. Due to antiinflammatory effects of gold, we have investigated the cerebral effects of metallic gold particles following a focal brain injury (freeze-lesion) in mice. Gold particles 20-45 microm in size or the vehicle (placebo) were implanted in the cortical tissue followed by a cortical freeze-lesioning. At 1-2 weeks post-injury, brains were analyzed by using immunohistochemistry and markers of inflammation, oxidative stress and apoptosis. This study shows that gold treatment significantly reduces the cerebral levels of tumor necrosis factor alpha (TNFalpha), oxidative DNA damage (as judged by 8-oxoguanine levels), and pro-apoptotic markers (cleaved caspase-3, cytochrome c leakage), when compared to those of controls. The data presented here points toward gold particles as a tool to modulate the cerebral response to injury.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / drug effects*
  • Apoptosis / physiology
  • Biomarkers / analysis
  • Biomarkers / metabolism
  • Brain Injuries / drug therapy*
  • Brain Injuries / metabolism
  • Brain Injuries / physiopathology
  • Caspase 3 / metabolism
  • Cerebral Cortex / drug effects
  • Cerebral Cortex / metabolism
  • Cerebral Cortex / pathology
  • Cytochromes c / metabolism
  • DNA Damage / drug effects
  • DNA Damage / physiology
  • Disease Models, Animal
  • Down-Regulation / drug effects
  • Down-Regulation / physiology
  • Female
  • Gold / pharmacology*
  • Gold / therapeutic use
  • Guanine / analogs & derivatives
  • Guanine / analysis
  • Guanine / metabolism
  • Immunohistochemistry
  • Mice
  • Mice, Inbred C57BL
  • Neurons / drug effects
  • Neurons / metabolism
  • Neurons / pathology
  • Neuroprotective Agents / pharmacology*
  • Neuroprotective Agents / therapeutic use
  • Oxidative Stress / drug effects*
  • Oxidative Stress / physiology
  • Treatment Outcome
  • Tumor Necrosis Factor-alpha / drug effects*
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Biomarkers
  • Neuroprotective Agents
  • Tumor Necrosis Factor-alpha
  • 8-hydroxyguanine
  • Guanine
  • Gold
  • Cytochromes c
  • Casp3 protein, mouse
  • Caspase 3