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

被引：6

作者：

Lyu, Dayin ^{[1
]}

Tian, Qing ^{[2
]}

Qian, Huitao ^{[3
]}

He, Chang ^{[1
]}

Shen, Tianyu ^{[4
]}

Xi, Jinxing ^{[5
]}

Xiao, Pingxi ^{[6
]}

Lu, Qiulun ^{[1
]}

机构：

[1] Nanjing Med Univ, Collaborat Innovat Ctr Cardiovasc Dis Translat Me, Key Lab Cardiovasc & Cerebrovasc Med, Nanjing 211166, Peoples R China

[2] Wuhan Asia Heart Hosp, Intens Care Unit, Wuhan 430000, Peoples R China

[3] Nanjing Med Univ, Clin Med Coll 1, Nanjing 211166, Peoples R China

[4] Hubei Univ Med, Taihe Hosp, Dept Orthoped Surg, Shiyan 442000, Peoples R China

[5] Nanjing Vocat Coll Informat Technol, Nanjing 211166, Peoples R China

[6] Nanjing Med Univ, Sir Runrun Hosp, Cardiac Dept, Nanjing 211166, Peoples R China

来源：

OXIDATIVE MEDICINE AND CELLULAR LONGEVITY | 2021年 / 2021卷

基金：

中国国家自然科学基金;

关键词：

ISCHEMIA-REPERFUSION INJURY; OXIDATIVE STRESS; ISCHEMIA/REPERFUSION INJURY; ROS;

D O I：

10.1155/2021/3766919

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

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.

引用

页数：8

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