Quercetin Protects H9c2 Cardiomyocytes against Oxygen-Glucose Deprivation/Reoxygenation-Induced Oxidative Stress and Mitochondrial Apoptosis by Regulating the ERK1/2/DRP1 Signaling Pathway

Fen Li; Dongsheng Li; Shifan Tang; Jianguang Liu; Jie Yan; Haifeng Chen; Xisheng Yan

doi:10.1155/2021/7522175

Quercetin Protects H9c2 Cardiomyocytes against Oxygen-Glucose Deprivation/Reoxygenation-Induced Oxidative Stress and Mitochondrial Apoptosis by Regulating the ERK1/2/DRP1 Signaling Pathway

Evid Based Complement Alternat Med. 2021 Aug 19:2021:7522175. doi: 10.1155/2021/7522175. eCollection 2021.

Authors

Fen Li¹, Dongsheng Li², Shifan Tang², Jianguang Liu¹, Jie Yan³, Haifeng Chen⁴, Xisheng Yan²

Affiliations

¹ Department of Neurology, Wuhan Third Hospital & Tongren Hospital of Wuhan University, Wuhan 430074, China.
² Department of Cardiology, Wuhan Third Hospital & Tongren Hospital of Wuhan University, Wuhan 430074, China.
³ Department of Forensic Science, Changsha 410013, China.
⁴ Department of Clinical Medicine, Jianghan University, Wuhan 430056, China.

Abstract

Reperfusion of blood flow during ischemic myocardium resuscitation induces ischemia/reperfusion (I/R) injury. Oxidative stress has been identified as a major cause in this process. Quercetin (QCT) is a member of the flavonoid family that exerts antioxidant effects. The aim of this study was to investigate the preventive effects of QCT on I/R injury and its underlying mechanism. To this end, H9c2 cardiomyocytes were treated with different concentrations of QCT (10, 20, and 40 μM) and subsequently subjected to oxygen-glucose deprivation/reperfusion (OGD/R) administration. The results indicated that OGD/R-induced oxidative stress, apoptosis, and mitochondrial dysfunction in H9c2 cardiomyocytes were aggravated following 40 μM QCT treatment and alleviated following the administration of 10 and 20 μM QCT prior to OGD/R treatment. In addition, OGD/R treatment inactivated ERK1/2 signaling activation. The effect was mitigated using 10 and 20 μM QCT prior to OGD/R treatment. In conclusion, these results suggested that low concentrations of QCT might alleviate I/R injury by suppressing oxidative stress and improving mitochondrial function through the regulation of ERK1/2-DRP1 signaling, providing a potential candidate for I/R injury prevention.