Mechanism for the protective effect of resveratrol against oxidative stress-induced neuronal death.
Mechanism for the protective effect of resveratrol against oxidative stress-induced neuronal death.
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DOI:
10.1016/j.freeradbiomed.2010.06.002
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发表时间:
2010-09-01
影响因子:
7.4
通讯作者:
Zhu, Bao Ting
中科院分区:
文献类型:
--
作者:
Fukui, Masayuki;Choi, Hye Joung;Zhu, Bao Ting
Oxidative stress can induce cytotoxicity in neurons, which plays an important role in the etiology of neuronal damage and degeneration. The present study seeks to determine the cellular and biochemical mechanisms underlying resveratrol’s protective effect against oxidative neuronal death. The cultured HT22 cells, an immortalized mouse hippocampal neuronal cell line, were used as an in vitro model, and the oxidative stress and neurotoxicity in these neuronal cells were induced by exposure to high concentrations of glutamate. Resveratrol strongly protected HT22 cells from glutamate-induced oxidative cell death. Resveratrol’s neuroprotective effect was independent of its direct radical-scavenging property, but instead was dependent on its ability to selectively induce the expression of mitochondrial superoxide dismutase (SOD2), and subsequently, reduce mitochondrial oxidative stress and damage. The induction of the mitochondrial SOD2 by resveratrol was mediated through the activation of the PI3K/Akt and GSK-3β/β-catenin signaling pathways. Taken together, the results of this study show that up-regulation of the mitochondrial SOD2 by resveratrol represents an important mechanism for its protection of neuronal cells against oxidative cytotoxicity resulting form mitochondrial oxidative stress.
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DOI:
10.1002/neu.480230915
发表时间:
1992-11-01
期刊:
JOURNAL OF NEUROBIOLOGY
影响因子:
--
作者:
CHOI, DW
通讯作者:
CHOI, DW
影响因子:
4.8
作者:
Horovitz-Fried, M;Cooper, DR;Sampson, SR
通讯作者:
Sampson, SR
影响因子:
4.8
作者:
Connor, KM;Subbaram, S;Melendez, JA
通讯作者:
Melendez, JA
影响因子:
3.7
作者:
Alvarez, AR;Godoy, JA;Inestrosa, NC
通讯作者:
Inestrosa, NC
影响因子:
2.8
作者:
Gill, Catherine;Walsh, Sinead E.;Watson, R. William G.
通讯作者:
Watson, R. William G.