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Attenuation of β-amyloid-induced oxidative cell death by sulforaphane via activation of NF-E2-related factor 2

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Affiliated Author(s)
이성용장정희
Alternative Author(s)
Lee, Seong RyongJang, Jung Hee
Journal Title
Oxidative Medicine and Cellular Longevity
ISSN
1942-0900
Issued Date
2013
Abstract
β-amyloid peptide (Aβ), a major component of senile plaques, plays important roles in neuropathology of Alzheimer's disease (AD). An array of in vitro and in vivo data indicates that Aβ-induced neuronal death is mediated by oxidative stress. In this study, we aimed to investigate effects of sulforaphane (SUL), an isothiocyanate in cruciferous vegetables, on Aβ-induced oxidative cell death in SH-SY5Y cells. Cells treated with Aβ25–35 exhibited decreased cell viability and underwent apoptosis as determined by MTT assay and TUNEL, respectively. Aβ25–35-induced cytotoxicity and apoptotic characteristics such as activation of c-JNK, dissipation of mitochondrial membrane potential, altered expression of Bcl-2 family proteins, and DNA fragmentation were effectively attenuated by SUL pretreatment. The antiapoptotic activity of SUL seemed to be mediated by inhibition of intracellular accumulation of reactive oxygen species and oxidative damages. SUL exerted antioxidant potential by upregulating expression of antioxidant enzymes including γ-glutamylcysteine ligase, NAD(P)H:quinone oxidoreductase-1, and heme oxygenase-1 via activation of NF-E2-related factor 2(Nrf2). The protective effect of SUL against Aβ25–35-induced apoptotic cell death was abolished by siRNA of Nrf2. Taken together, the results suggest that pharmacologic activation of Nrf2 signaling pathway by SUL might be a practical prevention and/or protective treatment for the management of AD.
Department
Dept. of Pharmacology (약리학)
Publisher
School of Medicine
Citation
Chan Lee et al. (2013). Attenuation of β-amyloid-induced oxidative cell death by sulforaphane via activation of NF-E2-related factor 2. Oxidative Medicine and Cellular Longevity, 2013, 313510–313510. doi: 10.1155%2F2013%2F313510
Type
Article
ISSN
1942-0900
DOI
10.1155%2F2013%2F313510
URI
https://kumel.medlib.dsmc.or.kr/handle/2015.oak/33625
Appears in Collections:
1. School of Medicine (의과대학) > Dept. of Pharmacology (약리학)
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