Ginsenoside Re rescues methamphetamine-induced oxidative damage, mitochondrial dysfunction, microglial activation, and dopaminergic degeneration by inhibiting the protein kinase Cδ gene

Eun Joo Shin, Seung Woo Shin, Thuy Ty Lan Nguyen, Dae Hun Park, Myung Bok Wie, Choon Gon Jang, Seung Yeol Nah, Byung Wook Yang, Sung Kwon Ko, Toshitaka Nabeshima, Hyoung Chun Kim

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Ginsenoside Re, one of the main constituents of Panax ginseng, possesses novel antioxidant and anti-inflammatory properties. However, the pharmacological mechanism of ginsenoside Re in dopaminergic degeneration remains elusive. We suggested that protein kinase C (PKC) δ mediates methamphetamine (MA)-induced dopaminergic toxicity. Treatment with ginsenoside Re significantly attenuated methamphetamine-induced dopaminergic degeneration in vivo by inhibiting impaired enzymatic antioxidant systems, mitochondrial oxidative stress, mitochondrial translocation of protein kinase Cδ, mitochondrial dysfunction, pro-inflammatory microglial activation, and apoptosis. These protective effects were comparable to those observed with genetic inhibition of PKCδ in PKCδ knockout (-/-) mice and with PKCδ antisense oligonucleotides, and ginsenoside Re did not provide any additional protective effects in the presence of PKCδ inhibition. Our results suggest that PKCδ is a critical target for ginsenoside Re-mediated protective activity in response to dopaminergic degeneration induced by MA.

Original languageEnglish
Pages (from-to)1400-1421
Number of pages22
JournalMolecular Neurobiology
Issue number3
Publication statusPublished - 06-2014


All Science Journal Classification (ASJC) codes

  • Neurology
  • Cellular and Molecular Neuroscience

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