Quercetin in Shengxian Decoction exhibits anti-ferroptosis protective roles in a myocardial infarction model via targeting DPP4/ HMOX1, based on network pharmacology and molecular docking

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Wydane w:Frontiers in Pharmacology vol. 16 (Apr 2025), p. 1583509-1583526
1. autor: Zhai, Yuming
Kolejni autorzy: Fu, Jiamei, Yang, Jianfei, Zhou, Yabin
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022 |a 1663-9812 
024 7 |a 1583509  |2 doi 
035 |a 3279124272 
045 2 |b d20250401  |b d20250430 
100 1 |a Zhai, Yuming  |u Graduate School, Heilongjiang University of Chinese Medicine, Harbin, Heilongjiang, China 
245 1 |a Quercetin in Shengxian Decoction exhibits anti-ferroptosis protective roles in a myocardial infarction model via targeting DPP4/ HMOX1, based on network pharmacology and molecular docking 
260 |b Frontiers Media SA  |c Apr 2025 
513 |a Journal Article 
520 3 |a BackgroundMyocardial infarction (MI) is characterized by high morbidity. In this study, we aimed to elucidate potential targets of Shengxian Decoction (SXD) against MI.MethodsPairing of SXD active ingredients and MI targets was conducted using the Chinese Medicine System Pharmacological Database, Gene Expression Omnibus (GEO), and STRING databases. The effects of SXD on MI were validated in vitro . Molecular docking was verified using cellular thermal shift assay (CETSA).ResultsA total of 40 active ingredients and 28 MI-related targets were obtained. Cross-analysis on 28 targets and cell death-related genes identified two crucial ferroptosis-related targets, namely, dipeptidyl peptidase 4 (DPP4) and heme oxygenase 1 (HMOX1). In cobalt chloride (CoCl2)-induced hypoxic H9c2 cells, SXD could remarkably improve cell viability and inhibit cell death. Meanwhile, SXD treatment significantly affected the ferroptosis-related markers in hypoxic H9c2 cells. Molecular docking and CETSA results showed that quercetin had good binding activity with DPP4 and HMOX1.ConclusionImportant active ingredient quercetin in SXD could exert anti-ferroptosis protective roles on MI through targeting ferroptosis-related genes (DPP4/HMOX1), thereby contributing to the protective role of SXD on MI. 
651 4 |a Beijing China 
651 4 |a China 
653 |a Databases 
653 |a Ferroptosis 
653 |a Cell death 
653 |a Morbidity 
653 |a Disease 
653 |a Mortality 
653 |a Heart failure 
653 |a Hypoxia 
653 |a Traditional Chinese medicine 
653 |a Drug development 
653 |a Computer simulation 
653 |a Pharmacology 
653 |a Cobalt chloride 
653 |a Myocardial infarction 
653 |a Genes 
653 |a Apoptosis 
653 |a Cell culture 
653 |a Drug dosages 
653 |a Proteins 
653 |a Heart attacks 
653 |a Permeability 
653 |a Cobalt 
653 |a Cardiomyocytes 
653 |a Pharmacokinetics 
653 |a Heme oxygenase (decyclizing) 
653 |a Gene expression 
653 |a Quercetin 
653 |a Cell viability 
653 |a Ischemia 
653 |a Cardiac function 
700 1 |a Fu, Jiamei  |u Department of Cardiovascular Medicine, The First Affiliated Hospital of Heilongjiang University of Chinese Medicine, Harbin, Heilongjiang, China 
700 1 |a Yang, Jianfei  |u Department of Cardiovascular Medicine, The First Affiliated Hospital of Heilongjiang University of Chinese Medicine, Harbin, Heilongjiang, China 
700 1 |a Zhou, Yabin  |u Department of Cardiovascular Medicine, The First Affiliated Hospital of Heilongjiang University of Chinese Medicine, Harbin, Heilongjiang, China 
773 0 |t Frontiers in Pharmacology  |g vol. 16 (Apr 2025), p. 1583509-1583526 
786 0 |d ProQuest  |t Biological Science Database 
856 4 1 |3 Citation/Abstract  |u https://www.proquest.com/docview/3279124272/abstract/embedded/L8HZQI7Z43R0LA5T?source=fedsrch 
856 4 0 |3 Full Text  |u https://www.proquest.com/docview/3279124272/fulltext/embedded/L8HZQI7Z43R0LA5T?source=fedsrch 
856 4 0 |3 Full Text - PDF  |u https://www.proquest.com/docview/3279124272/fulltextPDF/embedded/L8HZQI7Z43R0LA5T?source=fedsrch