Abstract
Quercetin has attracted more attention in recent years due to its protective role against ischemia/reperfusion injury. Quercetin can alleviate oxidative stress injury through the inhibition of NADPH oxidase and xanthine oxidase, blockage of the Fenton reaction, and scavenging of reactive oxygen species. Quercetin can also exert anti-inflammatory and anti-apoptotic effects by reducing the response to inflammatory factors and inhibiting cell apoptosis. Moreover, it can induce vasodilation effects through the inhibition of endothelin-1 receptors, the enhancement of NO stimulation and the activation of the large-conductance calcium-activated potassium channels. Finally, Quercetin can also antagonize the calcium overload. These multifaceted activities of Quercetin make it a potential therapeutic alternative for the treatment of ischemia/reperfusion injury.
Highlights
Quercetin (Que) is a flavonoid that is commonly found in fruits, vegetables, leaves, and Chinese herbs
In 2010, Que supplements were added to Food and Drug Administration’s Generally Recognized as Safe (GRAS) list at the dosage of 500 mg, which was recognized as an effective dosage in many trials (Dabeek and Marra, 2019)
NADPH oxidase can be activated by various agonists and stimulating factors (Anilkumar et al, 2009), such as G-protein-coupled receptors agonists, growth factors [thrombin and vascular endothelial growth factor (VEGF), cytokines tumor necrosis factor (TNF), and transforming growth factor (TGF)], mechanical injury, metabolism related factors, and ischemia reperfusion
Summary
Quercetin (Que) is a flavonoid that is commonly found in fruits, vegetables, leaves, and Chinese herbs. It is highly present in daily human aliment, such as onions, apple, red wine and tea, which are taken daily by human beings (Wang et al, 2019). It exerts various biological effects including antioxidant, anticancer, anti-inflammatory, anti-aggregatory, anti-aging effects (Iskender et al, 2017). Que has been recently shown to have prominent potentials to ameliorate myocardial damage under ischemia/reperfusion (I/R) condition through various pathways. We discuss the potential protective mechanisms of Que against myocardial I/R injury
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