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

Quercetin Protects H9c2 Cardiomyocytes against Oxygen-Glucose Deprivation/Reoxygenation-Induced Oxidative Stress and Mitochondrial Apoptosis by Regulating the ERK1/2/DRP1 Signaling Pathway.
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槲皮素通过调节 ERK1/2/DRP1 信号通路保护 H9c2 心肌细胞免受缺氧/复氧诱导的氧化应激和线粒体凋亡。

DOI:
10.1155/2021/7522175
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发表时间:
2021
期刊:
Evidence-based complementary and alternative medicine : eCAM
影响因子:
--
通讯作者:
Yan X
Yan X
中科院分区:
其他
文献类型:
--
作者:
Li F;Li D;Tang S;Liu J;Yan J;Chen H;Yan X

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缺血心肌复苏过程中的血流再灌注可引起缺血/再灌注(I/R)损伤。氧化应激已被确定为这一过程的主要原因。槲皮素(QCT)是类黄酮家族的一员,发挥抗氧化作用。本研究的目的是探讨QCT对I/R损伤的预防作用及其机制。为此,用不同浓度的QCT(10、20和40 μM)处理H9 c2心肌细胞,随后进行氧-葡萄糖剥夺/再灌注(OGD/R)给药。结果表明,OGD/R诱导的H9 c2心肌细胞氧化应激、凋亡和线粒体功能障碍在40 μM QCT处理后加重,在OGD/R处理前给予10和20 μM QCT后减轻。此外,OGD/R处理使ERK 1/2信号转导激活失活。在OGD/R处理前,使用10和20 μM QCT可减轻该效应。结论:低浓度QCT可能通过调节ERK 1/2-DRP 1信号通路抑制氧化应激,改善线粒体功能,从而减轻I/R损伤,为I/R损伤的预防提供了潜在的候选药物。
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.
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