Publication:
Melatonin reduces induction of Bax, caspase and cell death in methamphetamine-treated human neuroblastoma SH-SY5Y cultured cells

2
0

Issued Date

2009

Resource Type

Article

File Type

application/pdf

ISSN

7423098

DOI

10.1111/j.1600-079X.2009.00680.x

Other identifier(s)

2-s2.0-64649097900

Rights Holder(s)

Scopus

Bibliographic Citation

Journal of Pineal Research. Vol 46, No.4 (2009), p.433-440

Suggested Citation

Wisessmith W., Phansuwan-Pujito P., Govitrapong P., Chetsawang B. Melatonin reduces induction of Bax, caspase and cell death in methamphetamine-treated human neuroblastoma SH-SY5Y cultured cells. Journal of Pineal Research. Vol 46, No.4 (2009), p.433-440. doi:10.1111/j.1600-079X.2009.00680.x Retrieved from: https://hdl.handle.net/20.500.14740/6958

Title

Melatonin reduces induction of Bax, caspase and cell death in methamphetamine-treated human neuroblastoma SH-SY5Y cultured cells

Author(s)

Wisessmith W.
 Phansuwan-Pujito P.
 Govitrapong P.
 Chetsawang B.

Abstract

Several studies demonstrated that methamphetamine (MA)-treated human neuroblastoma cells exhibit increased oxidative stress, which regulates intracellular signaling cascades leading to cell death. Melatonin has a potential as a direct free radical scavenger and protects against cell death caused by MA. The objective of this study was to investigate the neuroprotective properties of melatonin on MA-induced induction of death signaling cascade and neuronal cell degeneration in human neuroblastoma SH-SY5Y cultured cells. The results of the present study demonstrate that MA significantly reduced cell viability in SH-SY5Y cultured cells. Desipramine, a monoamine uptake blocker, and melatonin reversed the toxic effect of MA in reducing cell viability. Induction of Bax, Bcl-2 and cleaved caspase-3 protein levels were observed in SH-SY5Y cultured cells treated with MA, whereas the induction of Bax and cleaved caspase-3 was diminished by melatonin. Visualization of the induction of Bax using immunofluorescence but a reduction in mitochondrial sites using red-fluorescent mitochondria-staining dye was more obviously apparent in MA-treated cells than in untreated control cells and, again, this effect was abolished by melatonin. These findings demonstrate important roles of Bax and caspase in death signaling cascade, and the protective effects of melatonin in MA-treated SH-SY5Y cells. © 2009 Blackwell Munksgaard.

Subject(s)

Caspase 3
 Desipramine
 Melatonin
 Methamphetamine
 Protein Bax
 Protein bcl 2
 Article
 Cell protection
 Cell viability
 Controlled study
 Enzyme degradation
 Human
 Human cell
 Mitochondrion
 Nerve cell degeneration
 Nerve cell necrosis
 Neuroblastoma cell
 Neuroprotection
 Bcl-2-Associated X Protein
 Caspase 3
 Cell Count
 Cell Death
 Cell Line, Tumor
 Cell Survival
 Desipramine
 Drug Interactions
 Humans
 Melatonin
 Methamphetamine
 Microscopy, Fluorescence
 Mitochondria
 Neuroblastoma
 Neuroprotective Agents
 Signal Transduction

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URI

https://hdl.handle.net/20.500.14740/6958

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Scopus: Year 1983-2021

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