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[6]-Gingerol attenuates β-amyloid-induced oxidative cell death via fortifying cellular antioxidant defense system

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Affiliated Author(s)
장정희
Alternative Author(s)
Jang, Jung Hee
Journal Title
Food and Chemical Toxicology
ISSN
0278-6915
Issued Date
2011
Abstract
b-Amyloid (Ab) is involved in the formation of senile plaques, the typical neuropathological marker for
Alzheimer’s disease (AD) and has been reported to cause apoptosis in neurons via oxidative and/or nitrosative
stress. In this study, we have investigated the neuroprotective effect and molecular mechanism of
[6]-gingerol, a pungent ingredient of ginger against Fb25–35-induced oxidative and/or nitrosative cell
death in SH-SY5Y cells. [6]-Gingerol pretreatment protected against Ab25–35-induced cytotoxicity and
apoptotic cell death such as DNA fragmentation, disruption of mitochondrial membrane potential, elevated
Bax/Bcl-2 ratio, and activation of caspase-3. To elucidate the neuroprotective mechanism of [6]-
gingerol, we have examined Ab25–35-induced oxidative and/or nitrosative stress and cellular antioxidant
defense system against them. [6]-Gingerol effectively suppressed Ab25–35-induced intracellular accumulation
of reactive oxygen and/or nitrogen species and restored Ab25–35-depleted endogenous antioxidant
glutathione levels. Furthermore, [6]-gingerol treatment up-regulated the mRNA and protein expression
of antioxidant enzymes such as c-glutamylcysteine ligase (GCL) and heme oxygenase-1 (HO-1), the rate
limiting enzymes in the glutathione biosynthesis and the degradation of heme, respectively. The expression
of aforementioned antioxidant enzymes seemed to be mediated by activation of NF-E2-related factor
2 (Nrf2). These results suggest that [6]-gingerol exhibits preventive and/or therapeutic potential for the
management of AD via augmentation of antioxidant capacity.
Department
Dept. of Pharmacology (약리학)
Publisher
School of Medicine
Citation
Chan Lee et al. (2011). [6]-Gingerol attenuates β-amyloid-induced oxidative cell death via fortifying
cellular antioxidant defense system. Food and Chemical Toxicology, 49(6), 1261–1269. doi: 10.1016/j.fct.2011.03.005
Type
Article
ISSN
0278-6915
DOI
10.1016/j.fct.2011.03.005
URI
https://kumel.medlib.dsmc.or.kr/handle/2015.oak/35743
Appears in Collections:
1. School of Medicine (의과대학) > Dept. of Pharmacology (약리학)
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