Oncotarget

Research Papers:

Gas signaling molecule hydrogen sulfide attenuates doxorubicin-induced dilated cardiomyopathy

Zongliang Yu, Wei Zhang, Mengyao Zhang, Mengchao Jin, Weiting Xu and Xiang Zhou _

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Oncotarget. 2017; 8:95425-95431. https://doi.org/10.18632/oncotarget.20729

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Abstract

Zongliang Yu1,*, Wei Zhang2,*, Mengyao Zhang1,*, Mengchao Jin2, Weiting Xu2 and Xiang Zhou2

1Department of Cardiology, The First People's Hospital of Kunshan Affiliated to Jiangsu University, Kunshan, China

2Department of Cardiology, The Second Affiliated Hospital of Soochow University, Suzhou, China

*These authors have contributed equally to this work

Correspondence to:

Xiang Zhou, email: zhou-xiang@suda.edu.cn

Keywords: hydrogen sulfide, doxorubicin, dilated cardiomyopathy, oxidative stress, apoptosis

Received: June 26, 2017     Accepted: August 09, 2017     Published: September 08, 2017

ABSTRACT

Increasing evidence has revealed that hydrogen sulfide (H2S) has beneficial effects in the treatment of various cardiovascular diseases. However, whether H2S can attenuate the development of dilated cardiomyopathy (DCM) remains unclear. In this study, we generated a rat model of DCM induced by doxorubicin and investigated the protective effects of H2S against DCM. Cardiac structure and function were analyzed by two-dimensional echocardiography. Oxidative stress was evaluated by measuring malondialdehyde, superoxide dismutase, glutathione peroxidase and reactive oxygen species. Cardiomyocyte apoptosis was assessed by flow cytometry following Annexin V/PI staining. Our results showed that exogenous administration of H2S could improve left ventricular structure and function in DCM rats. H2S was found to suppress doxorubicin-induced oxidative stress by activating the Nrf2 pathway and upregulating the expression of antioxidant proteins NQO1 and GCLM. Moreover, H2S was also found to inhibit doxorubicin-induced cardiomyocyte apoptosis by activating the PI3K/Akt signaling pathway. In conclusion, our study demonstrates that H2S protects against doxorubicin-induced DCM via attenuation of oxidative stress and apoptosis.


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