View : 30 Download: 3

Butin (7,3′,4′-trihydroxydihydroflavone) reduces oxidative stress-induced cell death via inhibition of the mitochondria-dependent apoptotic pathway

Title
Butin (7,3′,4′-trihydroxydihydroflavone) reduces oxidative stress-induced cell death via inhibition of the mitochondria-dependent apoptotic pathway
Authors
Zhang R.Lee I.K.Piao M.J.Kim K.C.Kim A.D.Kim H.S.Chae S.Hyun J.W.
Ewha Authors
김희선
SCOPUS Author ID
김희선scopus
Issue Date
2011
Journal Title
International Journal of Molecular Sciences
ISSN
1422-0067JCR Link
Citation
vol. 12, no. 6, pp. 3871 - 3887
Indexed
SCIE; SCOPUS WOS scopus
Abstract
Recently, we demonstrated that butin (7,3′,4′-trihydroxydihydroflavone) protected cells against hydrogen peroxide (H 2O 2)-induced apoptosis by: (1) scavenging reactive oxygen species (ROS), activating antioxidant enzymes such superoxide dismutase and catalase; (2) decreasing oxidative stress-induced 8-hydroxy-2′-deoxyguanosine levels via activation of oxoguanine glycosylase 1, and (3), reducing oxidative stress-induced mitochondrial dysfunction. The objective of this study was to determine the cytoprotective effects of butin on oxidative stress-induced mitochondria-dependent apoptosis, and possible mechanisms involved. Butin significantly reduced H 2O 2-induced loss of mitochondrial membrane potential as determined by confocal image analysis and flow cytometry, alterations in Bcl-2 family proteins such as decrease in Bcl-2 expression and increase in Bax and phospho Bcl-2 expression, release of cytochrome c from mitochondria into the cytosol and activation of caspases 9 and 3. Furthermore, the anti-apoptotic effect of butin was exerted via inhibition of mitogen-activated protein kinase kinase-4, c-Jun NH2-terminal kinase (JNK) and activator protein-1 cascades induced by H 2O 2 treatment. Finally, butin exhibited protective effects against H 2O 2-induced apoptosis, as demonstrated by decreased apoptotic bodies, sub-G 1 hypodiploid cells and DNA fragmentation. Taken together, the protective effects of butin against H 2O 2-induced apoptosis were exerted via blockade of membrane potential depolarization, inhibition of the JNK pathway and mitochondria-involved caspase-dependent apoptotic pathway. © 2011 by the authors; licensee MDPI, Basel, Switzerland.
DOI
10.3390/ijms12063871
Appears in Collections:
의학전문대학원 > 의학과 > Journal papers
Files in This Item:
001.pdf(619.49 kB)Download
Export
RIS (EndNote)
XLS (Excel)
XML


qrcode

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

BROWSE