Ginsenoside Rg1 attenuates dopamine-induced apoptosis in PC12 cells by suppressing oxidative stress

• Published in: European journal of pharmacology 2003-07, Vol.473 (1), p.1-7
• Main Authors: Chen, Xiao-Chun, Zhu, Yuan-Gui, Zhu, Li-An, Huang, Chun, Chen, Ying, Chen, Li-Min, Fang, Fang, Zhou, Yi-Can, Zhao, Chao-Hui
• Format: Article
• Language: English
• Subjects: Animals; Antioxidants - pharmacology; Apoptosis; Apoptosis - drug effects; Biological and medical sciences; Blotting, Western; Caspase 3; Caspase Inhibitors; Caspases - metabolism; Cytochrome c Group - drug effects; Cytochrome c Group - metabolism; DNA Fragmentation; Dopamine; Dopamine - metabolism; Dopamine - pharmacology; Flow Cytometry; Ginseng; Ginsenosides - pharmacology; Medical sciences; Neuroprotective Agents - pharmacology; Nitric Oxide - metabolism; Nitric Oxide Synthase - metabolism; Nitric Oxide Synthase Type II; Oxidative stress; Oxidative Stress - drug effects; Panax - chemistry; Parkinson's disease; PC12 Cells; Rats; Saponin
• ISSN: 0014-2999; 1879-0712
• DOI: 10.1016/S0014-2999(03)01945-9

In Parkinson's disease, neuroprotective therapy to rescue dopamine neurons has been proposed. Ginsenoside Rg1, one of the biologically active ingredients of ginseng, may be a candidate neuroprotective drug. In the present study, the mechanism underlying the neuroprotection provided by ginsenosde Rg1 was studied against apoptosis induced by exogenous dopamine in PC12 cells. Pretreatment with ginsenoside Rg1 markedly reduced the generation of dopamine-induced reactive oxygen species and the release of mitochondrial cytochrome c into the cytosol, and subsequently inhibited the activation of caspase-3. In addition, Rg1 pretreatment also reduced inducible nitric oxide (NO) synthase protein level and NO production. These results suggested that ginsenoside Rg1 may attenuate dopamine-induced apoptotic cell death through suppression of intracellular oxidative stress, and that it may rescue or protect dopamine neurons in Parkinson's disease.