抄録
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 |
| 巻 | 49 |
| 発行部数 | 3 |
| DOI | |
| 出版物ステータス | Published - 06-2014 |
| 外部発表 | Yes |
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All Science Journal Classification (ASJC) codes
- Neurology
- Cellular and Molecular Neuroscience
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Ginsenoside Re rescues methamphetamine-induced oxidative damage, mitochondrial dysfunction, microglial activation, and dopaminergic degeneration by inhibiting the protein kinase Cδ gene. / Shin, Eun Joo; Shin, Seung Woo; Nguyen, Thuy Ty Lan; Park, Dae Hun; Wie, Myung Bok; Jang, Choon Gon; Nah, Seung Yeol; Yang, Byung Wook; Ko, Sung Kwon; Nabeshima, Toshitaka; Kim, Hyoung Chun.
：: Molecular Neurobiology, 巻 49, 番号 3, 06.2014, p. 1400-1421.研究成果: Article
TY - JOUR
T1 - Ginsenoside Re rescues methamphetamine-induced oxidative damage, mitochondrial dysfunction, microglial activation, and dopaminergic degeneration by inhibiting the protein kinase Cδ gene
AU - Shin, Eun Joo
AU - Shin, Seung Woo
AU - Nguyen, Thuy Ty Lan
AU - Park, Dae Hun
AU - Wie, Myung Bok
AU - Jang, Choon Gon
AU - Nah, Seung Yeol
AU - Yang, Byung Wook
AU - Ko, Sung Kwon
AU - Nabeshima, Toshitaka
AU - Kim, Hyoung Chun
PY - 2014/6
Y1 - 2014/6
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=84902544775&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84902544775&partnerID=8YFLogxK
U2 - 10.1007/s12035-013-8617-1
DO - 10.1007/s12035-013-8617-1
M3 - Article
C2 - 24430743
AN - SCOPUS:84902544775
VL - 49
SP - 1400
EP - 1421
JO - Molecular Neurobiology
JF - Molecular Neurobiology
SN - 0893-7648
IS - 3
ER -