ReferenceID 5128

Dioscin Attenuates Myocardial Ischemic/Reperfusion-Induced Cardiac Dysfunction through Suppression of Reactive Oxygen Species

Oxid Med Cell Longev

Myocardial ischemic/reperfusion (MI/R) is a leading cause of cardiovascular disease with high morbidity and mortality. However, the mechanisms underlying pathological reperfusion remain obscure. In this study, we found t

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Reference Id
5128
Evidence Id
21718
Core Evidence Id
21718
Source Reference Id
3538
Herb2 Reference Id
HBREF004335
Subject Paper Key
HBIN024134_34664015
Pubmed Id
34664015
Doi
10.1155/2021/3766919
Paper Title
Dioscin Attenuates Myocardial Ischemic/Reperfusion-Induced Cardiac Dysfunction through Suppression of Reactive Oxygen Species
Paper Abstract
Myocardial ischemic/reperfusion (MI/R) is a leading cause of cardiovascular disease with high morbidity and mortality. However, the mechanisms underlying pathological reperfusion remain obscure. In this study, we found that dioscin, a natural product, could be a potential candidate for treating MI/R through modulating cardiac dysfunction. Mechanistically, our work revealed that dioscin could suppress the production of reactive oxygen species (ROS) via repressing the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 2 (Nox2) and enhancing the expression of antioxidant enzymes, including superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), and glutathione peroxidase (GPx). These findings indicate that dioscin may be a potential candidate for therapeutic interventions in MI/R injury.
Journal
Oxid Med Cell Longev
Publish Year
2021
Experiment Subject
Experiment Type
Animal Experiment
Phenotype Related
Cardiovascular Disease; Cardiac Dysfunction; Mi/r Injury; Myocardial Ischemic/reperfusion
Paper Title Cn
Paper Title En
Dioscin Attenuates Myocardial Ischemic/Reperfusion-Induced Cardiac Dysfunction through Suppression of Reactive Oxygen Species
Bilingual Status
semi_complete