Resveratrol attenuates 6-hydroxydopamine-induced oxidative damage and dopamine depletion in rat model of Parkinson's disease

Brain Res. 2010 Apr 30;1328:139-51. doi: 10.1016/j.brainres.2010.02.031. Epub 2010 Feb 16.


The present study was undertaken to investigate the neuroprotective effects of resveratrol (RES) on 6-hydroxydopamine (6-OHDA)-induced Parkinson's disease (PD) in rats. PD is an age-related neurodegenerative disorder in which the role of reactive oxygen species (ROS) is strongly implicated. RES, a polyphenolic antioxidant compound enriched in grapes, has been shown to have antioxidant and anti-inflammatory actions and thus was tested for its beneficial effects using 6-OHDA-induced PD rat model. Male Wistar rats were pretreated with RES (20mg/kg body weight i.p.) once daily for 15 days and subjected to unilateral intrastriatal injection of 6-OHDA (10 microg in 0.1% ascorbic acid in normal saline). Three weeks after 6-OHDA infusion, rats were tested for neurobehavioral activity and were killed after 4 weeks of 6-OHDA infusion for the estimation of lipid peroxidation, glutathione content, and activity of antioxidant enzymes (glutathione peroxidase [GPx], glutathione reductase [GR], catalase [CAT], and superoxide dismutase [SOD]. RES was found to be successful in upregulating the antioxidant status and lowering the dopamine loss. Conversely, the elevated level of thiobarbituric acid reactive substances (TBARS), protein carbonyl (PC), and activity of phospholipase A2 in 6-OHDA group was attenuated significantly in RES-pretreated group when compared with 6-OHDA-lesioned group. These results were supported by the immunohistochemical findings in the substantia nigra that has shown the protection of neurons by RES from deleterious effects of 6-OHDA. Thus, RES may be used to reduce the deterioration caused by free radicals thereby preventing subsequent behavioral, biochemical, and histopathological changes that occur during PD.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antioxidants / pharmacology
  • Antioxidants / therapeutic use
  • Disease Models, Animal
  • Dopamine / deficiency*
  • Enzymes / drug effects
  • Enzymes / metabolism
  • Free Radicals / metabolism
  • Glutathione / metabolism
  • Lipid Peroxidation / drug effects
  • Lipid Peroxidation / physiology
  • Male
  • Nerve Degeneration / chemically induced
  • Nerve Degeneration / drug therapy*
  • Nerve Degeneration / physiopathology
  • Neurotoxins / toxicity
  • Oxidative Stress / drug effects*
  • Oxidative Stress / physiology
  • Oxidopamine / toxicity
  • Parkinsonian Disorders / chemically induced
  • Parkinsonian Disorders / drug therapy*
  • Parkinsonian Disorders / physiopathology
  • Phospholipases A2 / metabolism
  • Rats
  • Rats, Wistar
  • Resveratrol
  • Stilbenes / pharmacology*
  • Stilbenes / therapeutic use
  • Substantia Nigra / drug effects
  • Substantia Nigra / metabolism
  • Substantia Nigra / physiopathology
  • Thiobarbituric Acid Reactive Substances / metabolism
  • Treatment Outcome


  • Antioxidants
  • Enzymes
  • Free Radicals
  • Neurotoxins
  • Stilbenes
  • Thiobarbituric Acid Reactive Substances
  • Oxidopamine
  • Phospholipases A2
  • Glutathione
  • Resveratrol
  • Dopamine