Next Article in Journal
Inorganic-Organic Hybrid Nanomaterials for Therapeutic and Diagnostic Imaging Applications
Previous Article in Journal
Structural Characterization of Poly-L-lactic Acid (PLLA) and Poly(glycolic acid)(PGA) Oligomers
Article Menu

Export Article

Open AccessArticle
Int. J. Mol. Sci. 2011, 12(6), 3871-3887; https://doi.org/10.3390/ijms12063871

Butin (7,3′,4′-Trihydroxydihydroflavone) Reduces Oxidative Stress-Induced Cell Death via Inhibition of the Mitochondria-Dependent Apoptotic Pathway

1
School of Medicine and Applied Radiological Science Research Institute, Jeju National University, Jeju-si 690-756, Korea
2
Cancer Research Institute, Seoul National University College of Medicine, Seoul 110-799, Korea
3
Aging Research Center, Korea Institute of Oriental Medicine, Daejeon 305–811, Korea
4
Department of Neuroscience, College of Medicine, Ewha Womans University, Seoul 110-783, Korea
These authors contributed equally to this study.
*
Author to whom correspondence should be addressed.
Received: 7 April 2011 / Revised: 16 May 2011 / Accepted: 31 May 2011 / Published: 10 June 2011
(This article belongs to the Section Biochemistry, Molecular and Cellular Biology)
View Full-Text   |   Download PDF [619 KB, uploaded 19 June 2014]

Abstract

Recently, we demonstrated that butin (7,3′,4′-trihydroxydihydroflavone) protected cells against hydrogen peroxide (H2O2)-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 H2O2-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 H2O2 treatment. Finally, butin exhibited protective effects against H2O2-induced apoptosis, as demonstrated by decreased apoptotic bodies, sub-G1 hypodiploid cells and DNA fragmentation. Taken together, the protective effects of butin against H2O2-induced apoptosis were exerted via blockade of membrane potential depolarization, inhibition of the JNK pathway and mitochondria-involved caspase-dependent apoptotic pathway View Full-Text
Keywords: butin; oxidative stress; mitochondria-dependent apoptotic pathway butin; oxidative stress; mitochondria-dependent apoptotic pathway
This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).
SciFeed

Share & Cite This Article

MDPI and ACS Style

Zhang, R.; Lee, I.K.; Piao, M.J.; Kim, K.C.; Kim, A.D.; Kim, H.S.; Chae, S.; Kim, H.S.; Hyun, J.W. Butin (7,3′,4′-Trihydroxydihydroflavone) Reduces Oxidative Stress-Induced Cell Death via Inhibition of the Mitochondria-Dependent Apoptotic Pathway. Int. J. Mol. Sci. 2011, 12, 3871-3887.

Show more citation formats Show less citations formats

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]
Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top