Abstract：
: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.
journal_name
Neurochem Intjournal_title
Neurochemistry internationalauthors
Yamada T,Hashida K,Takarada-Iemata M,Matsugo S,Hori Odoi
10.1016/j.neuint.2011.09.005subject
Has Abstractpub_date
2011-12-01 00:00:00pages
1003-9issue
7eissn
0197-0186issn
1872-9754pii
S0197-0186(11)00324-Xjournal_volume
59pub_type
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journal_title：Neurochemistry international
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journal_title：Neurochemistry international
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journal_title：Neurochemistry international
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journal_title：Neurochemistry international
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