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

doi:10.1016/j.bmcl.2015.11.005

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 journal › Journal article › peer-review

49 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 language	English
Pages (from-to)	181-185
Number of pages	5
Journal	Bioorganic and Medicinal Chemistry Letters
Volume	26
Issue number	1
DOIs	https://doi.org/10.1016/j.bmcl.2015.11.005
Publication status	Published - 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

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

Access to Document

10.1016/j.bmcl.2015.11.005

Cite this

@article{bfa1beb41a3d4dbca20ed294e525f01b,

title = "Calycosin inhibits oxidative stress-induced cardiomyocyte apoptosis via activating estrogen receptor-α/β",

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.",

keywords = "Apoptosis, Calycosin, Cardiomyocyte, Estrogen receptor",

author = "Bin Liu and Jingzhi Zhang and Weihua Liu and Ningning Liu and Xiuqiong Fu and Kwan, {Hiu Yee} and Shaojun Liu and Benrong Liu and Shuangwei Zhang and Zhiling Yu and Shiming Liu",

note = "Funding Information: This study is supported by Hong Kong Scholar Program 2015 – China (No. XJ2014057 ), National Natural Science Foundation of China – China (Nos. 81302892 , 81373520 , 81400231 ), Guangdong Natural Science Foundation – China (Nos. S2013040016226 , 2014A030313495 ), Science and Technology Planning Project of Guangdong Province – China (Nos. 2011B061300059 , 2014A020221059 ), and China Postdoctoral Science Foundation – China (Nos. 2013M530363 , 2014T70799 ). ",

year = "2016",

month = jan,

day = "1",

doi = "10.1016/j.bmcl.2015.11.005",

language = "English",

volume = "26",

pages = "181--185",

journal = "Bioorganic and Medicinal Chemistry Letters",

issn = "0960-894X",

publisher = "Elsevier Ltd.",

number = "1",

}

TY - JOUR

T1 - Calycosin inhibits oxidative stress-induced cardiomyocyte apoptosis via activating estrogen receptor-α/β

AU - Liu, Bin

AU - Zhang, Jingzhi

AU - Liu, Weihua

AU - Liu, Ningning

AU - Fu, Xiuqiong

AU - Kwan, Hiu Yee

AU - Liu, Shaojun

AU - Liu, Benrong

AU - Zhang, Shuangwei

AU - Yu, Zhiling

AU - Liu, Shiming

N1 - Funding Information: This study is supported by Hong Kong Scholar Program 2015 – China (No. XJ2014057 ), National Natural Science Foundation of China – China (Nos. 81302892 , 81373520 , 81400231 ), Guangdong Natural Science Foundation – China (Nos. S2013040016226 , 2014A030313495 ), Science and Technology Planning Project of Guangdong Province – China (Nos. 2011B061300059 , 2014A020221059 ), and China Postdoctoral Science Foundation – China (Nos. 2013M530363 , 2014T70799 ).

PY - 2016/1/1

Y1 - 2016/1/1

N2 - 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.

AB - 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.

KW - Apoptosis

KW - Calycosin

KW - Cardiomyocyte

KW - Estrogen receptor

UR - http://www.scopus.com/inward/record.url?scp=84949684396&partnerID=8YFLogxK

U2 - 10.1016/j.bmcl.2015.11.005

DO - 10.1016/j.bmcl.2015.11.005

M3 - Journal article

C2 - 26620254

AN - SCOPUS:84949684396

SN - 0960-894X

VL - 26

SP - 181

EP - 185

JO - Bioorganic and Medicinal Chemistry Letters

JF - Bioorganic and Medicinal Chemistry Letters

IS - 1

ER -

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

Abstract

Scopus Subject Areas

User-Defined Keywords

UN SDGs

Access to Document

Other files and links

Fingerprint

Cite this