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

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• 作者：Bin Liu^a ; ^b ; ^c ; ^&dagger ; ; Jingzhi Zhang^a ; ^&dagger ; ; Weihua Liu^a ; ^&dagger ; ; Ningning Liu^a ; Xiuqiong Fu^b ; Hiuyee Kwan^b ; Shaojun Liu^a ; Benrong Liu^a ; Shuangwei Zhang^a ; Zhiling Yu^b ; ^{zlyu@hkbu.edu.hk" class="auth_mail" title="E-mail the corresponding author} ; Shiming Liu^a ; ^{gzliushiming@126.com" class="auth_mail" title="E-mail the corresponding author}
• 关键词：Calycosin ; Apoptosis ; Cardiomyocyte ; Estrogen receptor
• 刊名：Bioorganic & Medicinal Chemistry Letters
• 出版年：2016
• 出版时间：1 January 2016
• 年：2016
• 卷：26
• 期：1
• 页码：181-185
• 全文大小：1756 K

文摘

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.