Biotargets for mediation of arsenic-induced coronary heart disease by calycosin

Arsenic (As), an environmental pollutant, is a highly poisonous metalloid. Accumulated evidence has shown the association between As exposure and elevated risk of the development of coronary heart disease (CHD). Calycosin, a beneficial flavonoid, has demonstrated cardioprotective activities, includi...

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Bibliographic Details
Published in:Food and agricultural immunology 2022-12, Vol.33 (1), p.207-219
Main Authors: Xu, Hongyuan, Qin, Lixiu, Nie, Litao, Li, Lin, Guo, Peng, Chen, Yizhao, Huang, Chuang, Su, Min, Yang, Bin
Format: Article
Language:English
Subjects:
Arsenic
Biotarget
Calycosin
Cardiovascular disease
Cardiovascular diseases
Coronary artery disease
Coronary heart disease
Epidermal growth factor
Flavonoids
Growth factors
Heart diseases
Interleukin 6
Kinases
MAP kinase
Molecular docking
Molecular modelling
Network pharmacology
Pharmacology
Pollutants
Protein kinase
Toxicity
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Summary:Arsenic (As), an environmental pollutant, is a highly poisonous metalloid. Accumulated evidence has shown the association between As exposure and elevated risk of the development of coronary heart disease (CHD). Calycosin, a beneficial flavonoid, has demonstrated cardioprotective activities, including those against CHD, in preclinical studies. The anti-As-related CHD activity and mechanism of calycosin have not yet been elucidated. Here, we aimed to determine the core biotargets and molecular mechanisms of calycosin against As-interrelated CHD via integrated bioinformatic analysis, including network pharmacology and molecular docking. The network pharmacology data demonstrated 41 intersection genes of calycosin against As-related CHD, prior to the identification of 15 core targets. Additional in silico investigation indicated that mitogen-activated protein kinase-3 (MAPK3), epidermal growth factor receptor (EGFR), and interleukin-6 (IL6) were the primary pharmacological targets of calycosin for the treatment of As-related CHD. In addition, the therapeutic effects can be realized via cardioprotection-associated signaling pathways for reducing As-induced myocardial toxicity and impairment and boosting CHD functional reparation. In summary, calycosin mediates potent pharmacological effects in As-related CHD therapy functioning via multiple targets and multiple pathways. The results may eventually aid in promoting future clinical application after experimental verification.
ISSN:0954-0105
1465-3443
DOI:10.1080/09540105.2022.2053947