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Cardiovascular Research Advance Access [Accepted Manuscript] published online on July 16, 2008
Cardiovascular Research, doi:10.1093/cvr/cvn192
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org

Ginkgo Biloba Extract 761 Reduces Doxorubicin-Induced Apoptotic Damage in Rat Hearts and Neonatal Cardiomyocytes

Tsun-Jui Liua,b, Yueh-Chiao Yeha, Chih-Tai Tinga,b, Wen-Lieng Leea,b, Li-Chuan Wanga, Hsiao-Wei Leea, Kuo-Yang Wanga,c, Hui-Chun Laid and Hui-Chin Laia,b,*

a Cardiovascular Center, Taichung Veterans General Hospital, Taichung
b Department of Medicine, Surgery and Cardiovascular Research Center, National Yang-Ming University, Taipei
c Department of Medicine, Chung-Shan Medical University, Taichung
d Chang-Gung Memorial Hospital and Chang-Gung University College of Medicine, Taoyuan, Linkoh, Taiwan

* Corresponding author: 160, Sec 3, Taichungkang Rd., Taichung, 407, Taiwan. Tel: +886-4-23592525 ext. 3131; Fax: +886-4-23599257. E-mail address: 854k{at}vghtc.gov.tw

Aims: The objective of this study was to investigate whether a cytoprotective herb-derived agent, Ginkgo biloba extract (EGb) 761, could have a beneficial effect on doxorubicin-induced cardiac toxicity in vitro and in vivo.

Methods and results: Primary cultured neonatal rat cardiomyocytes were treated with the vehicle, doxorubicin (1 µM), EGb761 (25 µg/ml), or EGb761 plus doxorubicin. After 24 hr, doxorubicin upregulated p53 mRNA expression, disturbed Bcl-2 family protein balance, disrupted mitochondrial membrane potential, precipitated mitochondrion-dependent apoptotic signaling, induced apoptotic cell death, and reduced viability of cardiomyocytes, whereas EGb761 pretreatment suppressed all the actions of doxorubicin. Similarly, rats treated with doxorubicin (3 mg/kg intraperitoneally 3 doses every other day) displayed retarded growth of body and heart as well as elevated apoptotic indexes in heart tissue at both 7 days and 28 days after exposure, while EGb761 pretreatment (5 mg/kg intraperitoneally 1 day before each dose of doxorubicin) effectively neutralized the aforementioned gross and cellular adverse effects of doxorubicin.

Conclusions: Doxorubicin impairs viability of cardiomyocytes at least partially by activating the p53-mediated, mitochondrion-dependent apoptotic signaling. EGb761 can effectively and extensively counteract this action of doxorubicin, and may potentially protect the heart from the severe toxicity of doxorubicin.

Time for primary review: 30 days

Tsun-Jui Liu and Yueh-Chiao Yeh contributed equally to this paper.


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