Publication:
Melatonin protects against hydrogen peroxide-induced cell death signaling in SH-SY5Y cultured cells: Involvement of nuclear factor kappa B, Bax and Bcl-2

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Issued Date

2006

Resource Type

Article

File Type

application/pdf

ISSN

7423098

DOI

10.1111/j.1600-079X.2006.00335.x

Other identifier(s)

2-s2.0-33746504821

Rights Holder(s)

Scopus

Bibliographic Citation

Journal of Pineal Research. Vol 41, No.2 (2006), p.116-123

Suggested Citation

Chetsawang B., Putthaprasart C., Phansuwan-Pujito P., Govitrapong P. Melatonin protects against hydrogen peroxide-induced cell death signaling in SH-SY5Y cultured cells: Involvement of nuclear factor kappa B, Bax and Bcl-2. Journal of Pineal Research. Vol 41, No.2 (2006), p.116-123. doi:10.1111/j.1600-079X.2006.00335.x Retrieved from: https://hdl.handle.net/20.500.14740/5564

Title

Melatonin protects against hydrogen peroxide-induced cell death signaling in SH-SY5Y cultured cells: Involvement of nuclear factor kappa B, Bax and Bcl-2

Author(s)

Chetsawang B.
 Putthaprasart C.
 Phansuwan-Pujito P.
 Govitrapong P.

Abstract

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.

Subject(s)

Acetylaspartylglutamylvalylaspartic acid
 Caspase inhibitor
 Hydrogen peroxide
 Hydroxyl radical
 Immunoglobulin enhancer binding protein
 Melatonin
 Protein Bax
 Protein bcl 2
 Reactive oxygen metabolite
 Superoxide
 Unclassified drug
 Article
 Cell damage
 Cell death
 Cell viability
 Controlled study
 Drug mechanism
 Enzyme activity
 Human
 Human cell
 Immunofluorescence
 Nerve cell degeneration
 Neuroblastoma cell
 Neuroprotection
 Oxidative stress
 Protein phosphorylation
 Active Transport, Cell Nucleus
 Antioxidants
 Bcl-2-Associated X Protein
 Blotting, Western
 Caspase 3
 Caspases
 Cell Death
 Cell Line, Tumor
 Humans
 Hydrogen Peroxide
 Melatonin
 Neurons
 Neuroprotective Agents
 NF-kappa B
 Oxidative Stress
 Phosphorylation
 Proto-Oncogene Proteins c-bcl-2
 Signal Transduction

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URI

https://hdl.handle.net/20.500.14740/5564

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Scopus: Year 1983-2021

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