Antioxidant nutrients and hypoxia/ischemia brain injury in rodents

Toxicology. 2003 Jul 15;189(1-2):55-61. doi: 10.1016/s0300-483x(03)00152-5.

Abstract

Cerebral ischemia and recirculation cause delayed neuronal death in rodents, such as Mongolian gerbils and stroke-prone spontaneously hypertensive rats (SHRSP), which were used as an experimental stroke model. It was documented that an enhanced nitric oxide production, the occurrence of apoptosis, and an attenuated redox regulatory system contribute to the development of delayed neuronal death. Many studies have suggested the beneficial antioxidant effects of antioxidant nutrients such as vitamin E, green tea extract, ginkgo biloba extract, resveratrol and niacin in cerebral ischemia and recirculation brain injury. These results are important in light of an attenuation of the deleterious consequences of oxidative stress in ischemia and recirculation injury.

Publication types

  • Review

MeSH terms

  • Animals
  • Antioxidants / pharmacology*
  • Brain / drug effects*
  • Brain / metabolism
  • Brain / pathology
  • Cell Death / drug effects
  • Disease Models, Animal
  • Gerbillinae
  • Ischemic Attack, Transient / metabolism
  • Ischemic Attack, Transient / pathology*
  • Neurons / drug effects*
  • Neurons / metabolism
  • Neurons / pathology
  • Nitric Oxide / metabolism
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • Rats
  • Rats, Inbred SHR
  • Reperfusion Injury / metabolism
  • Reperfusion Injury / pathology*
  • Reperfusion Injury / prevention & control
  • Thioredoxins / metabolism

Substances

  • Antioxidants
  • Proto-Oncogene Proteins c-bcl-2
  • Nitric Oxide
  • Thioredoxins