1. Academic Validation
  2. Salidroside Attenuates Doxorubicin-Induced Cardiac Dysfunction Partially Through Activation of QKI/FoxO1 Pathway

Salidroside Attenuates Doxorubicin-Induced Cardiac Dysfunction Partially Through Activation of QKI/FoxO1 Pathway

  • J Cardiovasc Transl Res. 2021 Apr;14(2):355-364. doi: 10.1007/s12265-020-10056-x.
Fangying Yan 1 Rongchen Liu 1 Xinyu Zhuang 1 Ruoshui Li 1 Haiming Shi 2 Xiufang Gao 3
Affiliations

Affiliations

  • 1 Department of Cardiology, Huashan Hospital, Fudan University, NO. 12 Middle Wulumuqi Road, Shanghai, 200000, China.
  • 2 Department of Cardiology, Huashan Hospital, Fudan University, NO. 12 Middle Wulumuqi Road, Shanghai, 200000, China. shihaiming_hs@163.com.
  • 3 Department of Cardiology, Huashan Hospital, Fudan University, NO. 12 Middle Wulumuqi Road, Shanghai, 200000, China. gaoxf_fudan@126.com.
Abstract

Doxorubicin (DOX) is an effective chemotherapy. However, its usage has been associated with adverse effects. Salidroside (SAL) is an antioxidative drug, which confers protective effects against several diseases. Salidroside can attenuate cardiac dysfunction induced by DOX. Quaking (QKI) is identified as a protective factor that can inhibit cardiotoxicity medicated by DOX through the regulation of cardiac circular RNA expression. The present study investigated the role of QKI on the protective effect of SAL in the DOX-induced cardiotoxicity model. Results indicated that SAL attenuated DOX-induced adverse effects, including cardiac dysfunction, weight loss, and Reactive Oxygen Species (ROS) production, and decreased the expression of Bax, Caspase 3, and FoxO1. Also, it increased the Mn-SOD2 and QKI expression in vivo and in vitro. Furthermore, QKI knockdown suppressed anti-cardiotoxicity mediated by SAL. In conclusion, the results of the current study show that salidroside attenuates doxorubicin-induced cardiac dysfunction through activation of QKI/FoxO1 pathway.

Keywords

Apoptosis; Doxorubicin; FoxO1; Quaking; Salidroside.

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