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ชื่อเรื่อง: Melatonin protects against hydrogen peroxide-induced cell death signaling in SH-SY5Y cultured cells: Involvement of nuclear factor kappa B, Bax and Bcl-2
ผู้แต่ง: Chetsawang B.
Putthaprasart C.
Phansuwan-Pujito P.
Govitrapong P.
Keywords: acetylaspartylglutamylvalylaspartic acid
caspase inhibitor
hydrogen peroxide
hydroxyl radical
immunoglobulin enhancer binding protein
protein Bax
protein bcl 2
reactive oxygen metabolite
unclassified drug
cell damage
cell death
cell viability
controlled study
drug mechanism
enzyme activity
human cell
nerve cell degeneration
neuroblastoma cell
oxidative stress
protein phosphorylation
Active Transport, Cell Nucleus
bcl-2-Associated X Protein
Blotting, Western
Caspase 3
Cell Death
Cell Line, Tumor
Hydrogen Peroxide
Neuroprotective Agents
NF-kappa B
Oxidative Stress
Proto-Oncogene Proteins c-bcl-2
Signal Transduction
วันที่เผยแพร่: 2006
บทคัดย่อ: Oxidative stress is defined as a disturbance in the prooxidant-antioxidant balance, leading to potential cell damage. Reactive oxygen species such as superoxide radicals, hydroxyl radicals and hydrogen peroxide may act also as secondary intermediaries in intracellular signaling leading to cell death. The neuroprotective effect of melatonin has been observed both in vivo and in vitro. The objective of this research, therefore, was to better understand the cellular mechanisms of neuronal cell degeneration induced via oxidative stress and the protective roles of melatonin on this cell death. In the present study, the effects of melatonin on H 2O 2-induced neuronal cell degeneration in human dopaminergic neuroblastoma SH-SY5Y cultured cells were investigated. The results showed that H 2O 2 significantly decreased cell viability and melatonin reversed the toxic effects of H 2O 2. An inhibition of caspase enzyme activity by Ac-DEVD-CHO, a caspase-3 inhibitor, significantly increased cell viability in H 2O 2-treated cells. The phosphorylation of transcription factors, nuclear factor kappa B (NF-κB) was increased in H 2O 2-treated cells and this effect was abolished by melatonin. Translocation of phosphorylated NF-κB to perinuclear and nuclear sites, estimated using immunofluorescence, occurred to a greater extent in H 2O 2-treated cells than in untreated control cells and again this effect was abolished by melatonin. In addition, induction of Bcl-2 and Bax proteins was demonstrated in SH-SY5Y cultured cells treated with H 2O 2, whereas the induction of Bax but not Bcl-2 was diminished by melatonin. In light of these finding, it is possible that the antioxidative stress effect of melatonin associated with inhibition of Bax expression, may offer a means of treating neuronal degeneration and disease. © 2006 The Authors.
ISSN: 7423098
Appears in Collections:Scopus 1983-2021

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