Anthocyanin attenuates doxorubicin-induced cardiomyotoxicity via estrogen receptor-α/β and stabilizes HSF1 to inhibit the IGF-IIR apoptotic pathway

Pei Chen Huang, Wei Wen Kuo, Chia Yao Shen, Yu Feng Chen, Yueh Min Lin, Tsung Jung Ho, V. Vijaya Padma, Jeng Fan Lo, Chih Yang Huang*

*此作品的通信作者

研究成果: Article同行評審

30 引文 斯高帕斯(Scopus)

摘要

Doxorubicin (Dox) is extensively used for chemotherapy in different types of cancer, but its use is limited to because of its cardiotoxicity. Our previous studies found that doxorubicin-induced insulin-like growth factor II receptor (IGF-IIR) accumulation causes cardiomyocytes apoptosis via down-regulation of HSF1 pathway. In these studies, we demonstrated a new mechanism through which anthocyanin protects cardiomyoblast cells against doxorubicin-induced injury. We found that anthocyanin decreased IGF-IIR expression via estrogen receptors and stabilized heat shock factor 1 (HSF1) to inhibit caspase 3 activation and apoptosis of cardiomyocytes. Therefore, the phytoestrogen from plants has been considered as another potential treatment for heart failure. It has been reported that the natural compound anthocyanin (ACN) has the ability to reduce the risk of cardiovascular disease (CVD). Here, we demonstrated that anthocyanin acts as a cardioprotective drug against doxorubicin-induced heart failure by attenuating cardiac apoptosis via estrogen receptors to stabilize HSF1 expression and down-regulated IGF-IIR-induced cardiomyocyte apoptosis.

原文English
文章編號1588
期刊International Journal Of Molecular Sciences
17
發行號9
DOIs
出版狀態Published - 21 9月 2016

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