2003年11月
Increase of antioxidative potential by tert-butylhydroquinone protects against cell death associated with 6-hydroxydopamine-induced oxidative stress in neuroblastoma SH-SY5Y cells
MOLECULAR BRAIN RESEARCH
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- 巻
- 119
- 号
- 2
- 開始ページ
- 125
- 終了ページ
- 131
- 記述言語
- 英語
- 掲載種別
- DOI
- 10.1016/j.molbrainres.2003.08.021
- 出版者・発行元
- ELSEVIER SCIENCE BV
Recent findings suggest that oxidative stress caused by dopamine could be closely involved in the pathogenesis of Parkinson's disease (PD). tert-Butylhydroquinone (tBHQ) is known as a strong inducer of phase 11 detoxification enzymes which have antioxidative functions. In this study, we investigated the neuroprotective effect of tBHQ against 6-hydroxydopamine (6-OHDA)-induced cell death using human neuroblastoma SH-SY5Y cells. The pretreatment of SH-SY5Y cells with tBHQ significantly reduced 6-OHDA-induced generation of reactive oxygen species (ROS), the phosphorylation of c-Jun N-terminal kinase (JNK), and subsequent cell death. We also observed that tBHQ increased the intracellular glutathione levels and induced the expression of NAD(P)H:quinone oxidoreductase (NQO1) mRNA. In addition, tBHQ dose-dependently activated the antioxidant responsive element (ARE), which plays a key role in the transcriptional activation of phase 11 detoxification enzymes including NQO1. These results indicate that an increase of intracellular antioxidative potential in SHSY5Y cells by tBHQ treatment protects cells from 6-OHDA-induced oxidative stress. (C) 2003 Elsevier B.V. All rights reserved.
- リンク情報
- ID情報
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- DOI : 10.1016/j.molbrainres.2003.08.021
- ISSN : 0169-328X
- Web of Science ID : WOS:000186852600001