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*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

30 Scopus citations

Abstract

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.

Original languageEnglish
Article number1588
JournalInternational Journal Of Molecular Sciences
Volume17
Issue number9
DOIs
StatePublished - 21 Sep 2016

Keywords

  • Anthocyanin
  • Apoptosis
  • Cardiomyocyte
  • Doxorubicin
  • Estrogen receptors
  • IGF-IIR signaling

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