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

• 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
• ISSN: 0954-0105; 1465-3443
• DOI: 10.1080/09540105.2022.2053947

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.