Neuroprotective effect of 20(S)-ginsenoside Rg3 on cerebral ischemia in rats

Neurosci Lett. 2005 Feb 10;374(2):92-7. doi: 10.1016/j.neulet.2004.10.030.

Abstract

This study was conducted to investigate the neuroprotective effects of 20(S)-ginsenoside Rg3 on focal cerebral ischemia in rats. Middle cerebral artery occlusion (MCAO) model in male Wistar-Kyoto (WKY) rats was employed. The behavioral tests were used to evaluate the damage to central nervous system. The infarct area of brain was assessed in the brain slices stained with 2,3,5-triphenyltetrazolium chloride (TTC). Hydrogen clearance techniques were used to monitor regional cerebral blood flow (rCBF), spectrophotometric assay methods were used to determine the activities of superoxide dismutase (SOD) and glutathione-peroxidase (GSH-Px), contents of malondialdehyde (MDA) and adenosine triphosphate (ATP) of the brain. Furthermore, the respiratory control ratio (RCR=State 3/State 4) was assessed in the brain mitochondria. The results showed that sublingual vein injection of 20(S)-ginsenoside Rg3 at doses of 10 and 5 mg kg(-1), but not 2.5 mg kg(-1) exhibited significant neuroprotective effects on rats against focal cerebral ischemic injury by markedly decreasing neurological deficit scores, reducing the infarct area and enhancing the rCBF compared with the control group. At the same time, 20(S)-ginsenoside Rg3 significantly improved mitochondrial energy metabolism, antagonized decreases in SOD and GSH-Px activities and increase in MDA level induced by cerebral ischemia. All these findings suggest that 20(S)-ginsenoside Rg3 might provide neuroprotection against the cerebral ischemia-induced injury in rat brain through reducing lipid peroxides, scavenging free radicals and improving the energy metabolism.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenosine Triphosphate / metabolism
  • Analysis of Variance
  • Animals
  • Brain Chemistry / drug effects
  • Brain Ischemia / etiology
  • Brain Ischemia / prevention & control*
  • Calcium Channel Blockers / therapeutic use
  • Cerebral Infarction / prevention & control
  • Disease Models, Animal
  • Dose-Response Relationship, Drug
  • Ginsenosides / therapeutic use*
  • Glutathione Peroxidase / metabolism
  • Infarction, Middle Cerebral Artery / complications
  • Male
  • Malondialdehyde / metabolism
  • Mitochondria / drug effects
  • Neurologic Examination / methods
  • Neuroprotective Agents / therapeutic use*
  • Nimodipine / therapeutic use
  • Rats
  • Rats, Inbred WKY
  • Superoxide Dismutase / metabolism
  • Time Factors

Substances

  • Calcium Channel Blockers
  • Ginsenosides
  • Neuroprotective Agents
  • ginsenoside Rg3
  • Malondialdehyde
  • Nimodipine
  • Adenosine Triphosphate
  • Glutathione Peroxidase
  • Superoxide Dismutase