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

研究成果: Article

73 引用 (Scopus)

抜粋

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.

元の言語English
ページ(範囲)1400-1421
ページ数22
ジャーナルMolecular Neurobiology
49
発行部数3
DOI
出版物ステータスPublished - 06-2014
外部発表Yes

All Science Journal Classification (ASJC) codes

  • Neurology
  • Cellular and Molecular Neuroscience

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    Shin, E. J., Shin, S. W., Nguyen, T. T. L., Park, D. H., Wie, M. B., Jang, C. G., Nah, S. Y., Yang, B. W., Ko, S. K., Nabeshima, T., & Kim, H. C. (2014). Ginsenoside Re rescues methamphetamine-induced oxidative damage, mitochondrial dysfunction, microglial activation, and dopaminergic degeneration by inhibiting the protein kinase Cδ gene. Molecular Neurobiology, 49(3), 1400-1421. https://doi.org/10.1007/s12035-013-8617-1