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α-Lipoic acid (LA) enantiomers protect SH-SY5Y cells against glutathione depletion
http://hdl.handle.net/2297/29609
http://hdl.handle.net/2297/29609aee5ff4b-4f8d-492e-8f35-7978b4d76ba3
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
ME-PR-HORI-O-1003.pdf (970.3 kB)
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| Item type | 学術雑誌論文 / Journal Article(1) | |||||
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| 公開日 | 2017-10-03 | |||||
| タイトル | ||||||
| タイトル | α-Lipoic acid (LA) enantiomers protect SH-SY5Y cells against glutathione depletion | |||||
| 言語 | ||||||
| 言語 | eng | |||||
| 資源タイプ | ||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
| 資源タイプ | journal article | |||||
| 著者 |
Yamada, Takashi
× Yamada, Takashi× Hashida, Koji× Takarada-Iemata, Mika× Matsugo, Seiichi× Hori, Osamu |
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| 書誌情報 |
Neurochemistry International 巻 59, 号 7, p. 1003-1009, 発行日 2011-12-01 |
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| ISSN | ||||||
| 収録物識別子タイプ | ISSN | |||||
| 収録物識別子 | 0197-0186 | |||||
| NCID | ||||||
| 収録物識別子タイプ | NCID | |||||
| 収録物識別子 | AA0032399X | |||||
| DOI | ||||||
| 関連タイプ | isVersionOf | |||||
| 識別子タイプ | DOI | |||||
| 関連識別子 | 10.1016/j.neuint.2011.09.005 | |||||
| 出版者 | ||||||
| 出版者 | Elsevier B.V. | |||||
| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | Growing evidence suggests that α-lipoic acid (LA) has neuroprotective effects in various pathological conditions including brain ischemia and neurodegeneration. While anti-oxidative activity has been thought to play a central role in LA-mediated neuroprotection, the precise mechanism and the effect of LA enantiomers (R- and S-LA) are not fully clarified. We, therefore, estimated the neuroprotective effects of LA against different cellular stresses including oxidative stress, endoplasmic reticulum (ER) stress and proteolytic stress using human neuroblastoma SH-SY5Y cells. All types of LAs (racemate, R-LA and S-LA) most effectively prevented cell death induced by buthionine sulfoximine (BSO) which depletes intracellular glutathione. Although direct effects of LA on glutathione depletion or generation of the reactive oxygen species (ROS) were relatively small upon BSO treatment, LA enhanced expressions of anti-oxidative genes such as heme oxygenase-1 (HO-1) and phase II detoxification enzymes such as NAD(P)H:Quinone Oxidoreductase 1 (NQO1). An inhibitor of NQO1, but not that of HO-1, suppressed LA-mediated protection against BSO. Further experiments revealed that all types of LAs activated cell survival-associated kinase Akt, and an inhibitor of PI3K, LY294002, suppressed both LA-induced upregulation of NQO1 and cell protection against BSO. Our results suggest an important role of PI3K/Akt-mediated upregulation of genes including phase II enzymes such as NQO1 in LA-mediated neuroprotection. © 2011 Elsevier B.V. | |||||
| 著者版フラグ | ||||||
| 出版タイプ | AM | |||||
| 出版タイプResource | http://purl.org/coar/version/c_ab4af688f83e57aa | |||||
| 関連URI | ||||||
| 識別子タイプ | URI | |||||
| 関連識別子 | http://www.elsevier.com/locate/issn/01970186 | |||||
