Calycosin inhibits oxidative stress-induced cardiomyocyte apoptosis via activating estrogen receptor-α/β

Bin Liu, Jingzhi Zhang, Weihua Liu, Ningning Liu, Xiuqiong FU, Hiu Yee KWAN, Shaojun Liu, Benrong Liu, Shuangwei Zhang, Zhiling YU*, Shiming Liu

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

28 Citations (Scopus)

Abstract

Oxidative stress-induced myocardial apoptosis is a key step in the pathogenesis of ischemic heart disease. Calycosin is a phytoestrogen extracted from Radix astragali. In this study, we examined the effects and mechanisms of calycosin on oxidative stress-induced myocardial apoptosis. Molecular docking showed that calycosin can couple into binding site of ERα and β. Pretreatment with calycosin increased the expression levels of ERα and β. In H9C2 cells, H2O2 reduced cell viability and induced apoptosis, however, calycosin diminished the effects of H2O2 in a dose-dependent manner. Pretreatment with ICI 182,780, an estrogen receptor inhibitor, negated the protective effect of calycosin against H2O2-induced apoptosis. In addition, Akt phosphorylation was upregulated by calycosin mono treatment and downregulated by co-treatment with calycosin and ICI 182,780. These data demonstrated that calycosin exhibits anti-apoptotic effects by activating ERα/β and enhancing Akt phosphorylation in cardiomyocytes.

Original languageEnglish
Pages (from-to)181-185
Number of pages5
JournalBioorganic and Medicinal Chemistry Letters
Volume26
Issue number1
DOIs
Publication statusPublished - 1 Jan 2016

Scopus Subject Areas

  • Biochemistry
  • Molecular Medicine
  • Molecular Biology
  • Pharmaceutical Science
  • Drug Discovery
  • Clinical Biochemistry
  • Organic Chemistry

User-Defined Keywords

  • Apoptosis
  • Calycosin
  • Cardiomyocyte
  • Estrogen receptor

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