Linked Life Data

16879316

Source:http://linkedlifedata.com/resource/pubmed/id/16879316

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2006-8-1
pubmed:abstractText
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(2)O(2)-induced neuronal cell degeneration in human dopaminergic neuroblastoma SH-SY5Y cultured cells were investigated. The results showed that H(2)O(2) significantly decreased cell viability and melatonin reversed the toxic effects of H(2)O(2). An inhibition of caspase enzyme activity by Ac-DEVD-CHO, a caspase-3 inhibitor, significantly increased cell viability in H(2)O(2)-treated cells. The phosphorylation of transcription factors, nuclear factor kappa B (NF-kappaB) was increased in H(2)O(2)-treated cells and this effect was abolished by melatonin. Translocation of phosphorylated NF-kappaB to perinuclear and nuclear sites, estimated using immunofluorescence, occurred to a greater extent in H(2)O(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(2)O(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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0742-3098
pubmed:author
pubmed:issnType
Print
pubmed:volume
41
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
116-23
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:16879316-Active Transport, Cell Nucleus, pubmed-meshheading:16879316-Antioxidants, pubmed-meshheading:16879316-Blotting, Western, pubmed-meshheading:16879316-Caspase 3, pubmed-meshheading:16879316-Caspases, pubmed-meshheading:16879316-Cell Death, pubmed-meshheading:16879316-Cell Line, Tumor, pubmed-meshheading:16879316-Humans, pubmed-meshheading:16879316-Hydrogen Peroxide, pubmed-meshheading:16879316-Melatonin, pubmed-meshheading:16879316-NF-kappa B, pubmed-meshheading:16879316-Neurons, pubmed-meshheading:16879316-Neuroprotective Agents, pubmed-meshheading:16879316-Oxidative Stress, pubmed-meshheading:16879316-Phosphorylation, pubmed-meshheading:16879316-Proto-Oncogene Proteins c-bcl-2, pubmed-meshheading:16879316-Signal Transduction, pubmed-meshheading:16879316-bcl-2-Associated X Protein
pubmed:year
2006
pubmed:articleTitle
Melatonin protects against hydrogen peroxide-induced cell death signaling in SH-SY5Y cultured cells: involvement of nuclear factor kappa B, Bax and Bcl-2.
pubmed:affiliation
Neuro-Behavioural Biology Center, Institute of Science and Technology for Research and Development, Mahidol University, Salaya, Nakornpathom, Thailand. grbcs@mahidol.ac.th
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't