Abstract
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.
| Original language | English |
|---|---|
| Pages (from-to) | 337-345 |
| Number of pages | 9 |
| Journal | Genes and Nutrition |
| Volume | 2 |
| Issue number | 4 |
| DOIs | |
| Publication status | Published - 2008 Feb 1 |
Fingerprint
Keywords
- Cardiomyocytes
- Cytoprotection
- Detoxification
- Doxorubicin
- Glutathione S-transferase
- Schisandra fructus
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism
- Genetics
Cite this
Schisandra fructus extract ameliorates doxorubicin-induce cytotoxicity in cardiomyocytes : Altered gene expression for detoxification enzymes. / Choi, Eun Hye; Lee, Nari; Kim, Hyun Jung; Kim, Mi Kyung; Chi, Sung-Gil; Kwon, Dae Young; Chun, Hyang Sook.
In: Genes and Nutrition, Vol. 2, No. 4, 01.02.2008, p. 337-345.Research output: Contribution to journal › Article
}
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
PY - 2008/2/1
Y1 - 2008/2/1
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
UR - http://www.scopus.com/inward/record.url?scp=41349117220&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=41349117220&partnerID=8YFLogxK
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 -