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; doi: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 Biology and Biophysics)
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 alert for new publications

Never miss any articles matching your research from any publisher
  • Get alerts for new papers matching your research
  • Find out the new papers from selected authors
  • Updated daily for 49'000+ journals and 6000+ publishers
  • Define your Scifeed now

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