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Cytoprotective effects of triphlorethol-A against formaldehyde-induced oxidative damage and apoptosis: Role of mitochondria-mediated caspase-dependent pathway

Title
Cytoprotective effects of triphlorethol-A against formaldehyde-induced oxidative damage and apoptosis: Role of mitochondria-mediated caspase-dependent pathway
Authors
Zhang R.Lee I.K.Kang K.A.Piao M.J.Kim K.C.Kim B.J.Lee N.H.Choi J.-Y.Choi J.Hyun J.W.
Ewha Authors
최정윤
Issue Date
2010
Journal Title
Journal of Toxicology and Environmental Health - Part A: Current Issues
ISSN
1528-7394JCR Link
Citation
vol. 73, no. 21-22, pp. 1477 - 1489
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
The toxicity of formaldehyde (HCHO) has been attributed to its ability to form adducts with DNA and proteins. Triphlorethol-A, derived from Ecklonia cava, was reported to exert a cytoprotective effect against oxidative stress damage via an antioxidant mechanism. The aim of this study was to examine the mechanisms underlying the triphlorethol-A ability to protect Chinese hamster lung fibroblast (V79-4) cells against HCHO-induced damage. Triphlorethol-A significantly decreased the HCHO-induced intracellular reactive oxygen species (ROS) production. Triphlorethol-A prevented increased cell damage induced by HCHO via inhibition of mitochondria-mediated caspase-dependent apoptosis pathway. Triphlorethol-A diminished HCHO-induced mitochondrial dysfunction, including loss of mitochondrial membrane action potential (Δψ) and adenosine triphosphate (ATP) depletion. Furthermore, the anti-apoptotic effect of triphlorethol-A was exerted through inhibition of c-Jun NH 2-terminal kinase (JNK), which was enhanced by HCHO. Our data indicate that triphlorethol-A exerts a cytoprotective effect in V79-4 cells against HCHO-induced oxidative stress by inhibiting the mitochondria-mediated caspase-dependent apoptotic pathway. Copyright © Taylor & Francis Group, LLC.
DOI
10.1080/15287394.2010.511564
Appears in Collections:
의학전문대학원 > 의학과 > Journal papers
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