Oncotarget

Research Papers:

Oral administration of Ginsenoside Rg1 prevents cardiac toxicity induced by doxorubicin in mice through anti-apoptosis

Chen Zhu, Yi Wang, Hua Liu, Haiman Mu, Yue Lu, Jiayi Zhang and Jianhua Huang _

PDF  |  HTML  |  How to cite

Oncotarget. 2017; 8:83792-83801. https://doi.org/10.18632/oncotarget.19698

Metrics: PDF 1640 views  |   HTML 3141 views  |   ?  


Abstract

Chen Zhu1,2,*, Yi Wang1,*, Hua Liu3, Haiman Mu1, Yue Lu2, Jiayi Zhang1 and Jianhua Huang1

1First Affiliated Hospital of Jinzhou Medical University, Jinzhou, China

2Graduated School of Jinzhou Medical University, Jinzhou, China

3Third Affiliated Hospital of Jinzhou Medical University, Jinzhou, China

*These authors have contributed equally to this work

Correspondence to:

Jianhua Huang, email: [email protected]

Hua Liu, email: [email protected]

Keywords: Rg1, cardiac toxicity, doxorubicin, apoptosis

Received: March 29, 2017     Accepted: June 28, 2017     Published: July 31, 2017

ABSTRACT

Although Ginsenoside Rg1 has been reported to have protective cardiac effects, its effects on cardiac toxicity induced by doxorubicin needs to be studied. The present study investigated the effects of oral administration of Rg1 on the heart in mice treated with doxorubicin and found improved fractional shortening and ejection fraction of the heart and decreased cardiac apoptosis in mice treated with doxorubicin. The underlying mechanisms include increased phosphorylation of Akt and Erk by Rg1, increased ratio of Bcl-2 and Bax, and decreased release of cytochrome c from mitochondria, thereby protecting the heart from doxorubicin-induced apoptosis. This phenotype suggested that the oral administration of Rg1 may be a potential method preventing the cardiac toxicity caused by doxorubicin in clinical practice.


Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 19698