PMID- 15659115 OWN - NLM STAT- MEDLINE DCOM- 20050616 LR - 20161124 IS - 1671-4083 (Print) IS - 1671-4083 (Linking) VI - 26 IP - 1 DP - 2005 Jan TI - Ginsenoside Rg1 reduces MPTP-induced substantia nigra neuron loss by suppressing oxidative stress. PG - 56-62 AB - AIM: 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. CONCLUSION: The antioxidant property of Rg1 along with the blocking of JNK signaling cascade might contribute to the neuroprotective effect of ginsenoside Rg1 against MPTP. FAU - Chen, Xiao-chun AU - Chen XC AD - Fujian Institute of Geriatrics, Union Hospital, Fujian Medical University, Fuzhou 350001, China. chenxc998@sohu.com FAU - Zhou, Yi-can AU - Zhou YC FAU - Chen, Ying AU - Chen Y FAU - Zhu, Yuan-gui AU - Zhu YG FAU - Fang, Fang AU - Fang F FAU - Chen, Li-min AU - Chen LM LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - United States TA - Acta Pharmacol Sin JT - Acta pharmacologica Sinica JID - 100956087 RN - 0 (Ginsenosides) RN - 0 (Neuroprotective Agents) RN - EC 1.15.1.1 (Superoxide Dismutase) RN - EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases) RN - GAN16C9B8O (Glutathione) RN - PJ788634QY (ginsenoside Rg1) SB - IM MH - Animals MH - *Apoptosis MH - Ginsenosides/isolation & purification/*pharmacology MH - Glutathione/metabolism MH - JNK Mitogen-Activated Protein Kinases/metabolism MH - *MPTP Poisoning/metabolism/pathology MH - Male MH - Mice MH - Mice, Inbred C57BL MH - Neurons/pathology MH - Neuroprotective Agents/pharmacology MH - Oxidative Stress/*drug effects MH - Panax/chemistry MH - Plants, Medicinal/chemistry MH - *Substantia Nigra/pathology MH - Superoxide Dismutase/metabolism EDAT- 2005/01/22 09:00 MHDA- 2005/06/17 09:00 CRDT- 2005/01/22 09:00 PHST- 2005/01/22 09:00 [pubmed] PHST- 2005/06/17 09:00 [medline] PHST- 2005/01/22 09:00 [entrez] AID - APHS019 [pii] AID - 10.1111/j.1745-7254.2005.00019.x [doi] PST - ppublish SO - Acta Pharmacol Sin. 2005 Jan;26(1):56-62. doi: 10.1111/j.1745-7254.2005.00019.x.