TY - JOUR
T1 - Schisandra fructus extract ameliorates doxorubicin-induce cytotoxicity in cardiomyocytes
T2 - Altered gene expression for detoxification enzymes
AU - Choi, Eun Hye
AU - Lee, Nari
AU - Kim, Hyun Jung
AU - Kim, Mi Kyung
AU - Chi, Sung Gil
AU - Kwon, Dae Young
AU - Chun, Hyang Sook
N1 - Funding Information:
Acknowledgments This work was supported by a research project on Functional Food Development from the Office for Government Policy Coordination, and by research grants from the Korea Institute of Science and Technology Evaluation and Planning (KISTEP) for functional food research and development, Ministry of Science and Technology, in the Republic of Korea.
Copyright:
Copyright 2009 Elsevier B.V., All rights reserved.
PY - 2008/2
Y1 - 2008/2
N2 - The effect of Schisandra fructus extract (SFE) on doxoruBicin (Dox)-induced cardiotoxicity was investigated in H9c2 cardiomyocytes. Dox, which is an antineoplastic drug known to induce cardiomyopathy possibly through production of reactive oxygen species, induced significant cytotoxicity, intracellular reactive oxygen species (ROS), and lipid peroxidation. SFE treatment significantly increased cell survival up to 25%, inhibited intracellular ROS production in a time- and dose-dependent manner, and inhibited lipid peroxidation induced by Dox. In addition, SFE treatment induced expression of cellular glutathione S-transferases (GSTs), which function in the detoxification of xenobiotics, and endogenous toxicants including lipid peoxides. Analyses of 31,100 genes using Affymetrix cDNA microarrays showed that SFE treatment up-regulated expression of genes involved in glutathione metabolism and detoxification [GST theta 1, mu 1, and alpha type 2, heme oxygenase 1 (HO-1), and microsomal epoxide hydrolase (mEH)] and energy metabolism [carnitine palmitoyltransferase-1 (CPT-1), transaldolase, and transketolase]. These data indicated that SFE might increase the resistance to cardiac cell injury by Dox, at least partly, together with altering gene expression, especially induction of phase II detoxification enzymes.
AB - The effect of Schisandra fructus extract (SFE) on doxoruBicin (Dox)-induced cardiotoxicity was investigated in H9c2 cardiomyocytes. Dox, which is an antineoplastic drug known to induce cardiomyopathy possibly through production of reactive oxygen species, induced significant cytotoxicity, intracellular reactive oxygen species (ROS), and lipid peroxidation. SFE treatment significantly increased cell survival up to 25%, inhibited intracellular ROS production in a time- and dose-dependent manner, and inhibited lipid peroxidation induced by Dox. In addition, SFE treatment induced expression of cellular glutathione S-transferases (GSTs), which function in the detoxification of xenobiotics, and endogenous toxicants including lipid peoxides. Analyses of 31,100 genes using Affymetrix cDNA microarrays showed that SFE treatment up-regulated expression of genes involved in glutathione metabolism and detoxification [GST theta 1, mu 1, and alpha type 2, heme oxygenase 1 (HO-1), and microsomal epoxide hydrolase (mEH)] and energy metabolism [carnitine palmitoyltransferase-1 (CPT-1), transaldolase, and transketolase]. These data indicated that SFE might increase the resistance to cardiac cell injury by Dox, at least partly, together with altering gene expression, especially induction of phase II detoxification enzymes.
KW - Cardiomyocytes
KW - Cytoprotection
KW - Detoxification
KW - Doxorubicin
KW - Glutathione S-transferase
KW - Schisandra fructus
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U2 - 10.1007/s12263-007-0073-y
DO - 10.1007/s12263-007-0073-y
M3 - Article
C2 - 18850228
AN - SCOPUS:41349117220
VL - 2
SP - 337
EP - 345
JO - Genes and Nutrition
JF - Genes and Nutrition
SN - 1555-8932
IS - 4
ER -
