title: Ginsenoside Rg1 reduces MPTP-induced substantia nigra neuron loss by suppressing oxidative stress.
abstract: OBJECTIVE
  To investigate the effect of ginsenoside Rg1, an effective ingredient from ginsenoside, on 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced substantia nigra neuron lesion.
  
  
  METHODS
  C57-BL mice were given MPTP to prepare Parkinson disease mice model. Different doses of Rg1 (5, 10, and 20 mg.kg(-1).d(-1)) or N-acetylcystein (NAC) (300 mg.kg(-1).d(-1)) were given 3 d prior to MPTP in the pretreatment groups. Glutathione (GSH) level and total superoxide dismutase (T-SOD) activity in substantia nigra were determined by spectrophotometry. Nissl staining, tyrosine hydroxylase immunostaining, and TUNEL labeling were used to observe the damage and apoptosis of nigral neurons. Western blot analysis was used to detect the phospho-JNK and phospho-c-Jun levels in midbrain homogenates.
  
  
  RESULTS
  Pretreatments of C57-BL mice with different doses of Rg1 or NAC were found to protect against MPTP-induced substantia nigra neurons loss. Rg1 or NAC prevented GSH reduction and T-SOD activation in substantia nigra, and attenuated the phosphorylations of JNK and c-Jun following MPTP treatment.
  
  
  CONCLUSIONS
  The antioxidant property of Rg1 along with the blocking of JNK signaling cascade might contribute to the neuroprotective effect of ginsenoside Rg1 against MPTP.
authors.affiliation: Fujian Institute of Geriatrics, Union Hospital, Fujian Medical University, Fuzhou 350001, China. chenxc998@sohu.com
authors.forename: Xiao-chun
authors.initials: XC
authors.lastname: Chen
authors.forename: Yi-can
authors.initials: YC
authors.lastname: Zhou
authors.forename: Ying
authors.initials: Y
authors.lastname: Chen
authors.forename: Yuan-gui
authors.initials: YG
authors.lastname: Zhu
authors.forename: Fang
authors.initials: F
authors.lastname: Fang
authors.forename: Li-min
authors.initials: LM
authors.lastname: Chen
mesh_terms: D000818:Animals; D017209:Apoptosis; D036145:Ginsenosides / Q000302:isolation & purification / Q000494:pharmacology*; D005978:Glutathione / Q000378:metabolism; D048031:JNK Mitogen-Activated Protein Kinases / Q000378:metabolism; D020267:MPTP Poisoning / Q000378:metabolism / Q000473:pathology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009474:Neurons / Q000473:pathology; D018696:Neuroprotective Agents / Q000494:pharmacology; D018384:Oxidative Stress / Q000187:drug effects*; D005894:Panax / Q000737:chemistry; D010946:Plants, Medicinal / Q000737:chemistry; D013378:Substantia Nigra / Q000473:pathology; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D036145:Ginsenosides; D018696:Neuroprotective Agents; D013482:Superoxide Dismutase; D048031:JNK Mitogen-Activated Protein Kinases; D005978:Glutathione; C035054:ginsenoside Rg1