Acute myocardial infarction (AMI) is the maximum critical cardiovascular event and causes high morbidity and mortality worldwide. The ischemia and reperfusion that occur in AMI cause apoptosis and cellular dysfunction in cardiomyocytes. IL-20, an IL-10 family member, is involved in various inflammatory diseases. Therefore, we sought to elucidate the role of IL-20 in the infarcted heart following ischemia/reperfusion (I/R) injury. We found that IL-20 and its receptors, IL-20R1 and IL-20R2, were increased in H2C2 cardiomyoblast cells and ventricular tissues subjected to hypoxia/reoxygenation (H/R) stimulation. The presence of IL-20 further inhibited the cell viability of H9C2 cells and primary cardiomyocytes. Our results suggested that IL-20 elicited an increase in Ca2+ and activation of the PKC/NADPH oxidase pathway, leading to the elevation of oxidase stress and downregulation of AKT. Furthermore, we demonstrated that IL-20 was able to mediate H/R-induced apoptosis via PKC/NADPH oxidase/AKT signaling. Our findings implied that IL-20 was responsive to H/R stress in vitro and in rat hearts undergoing I/R injury, and this upregulation of IL-20 may contribute to the apoptosis of cardiomyocytes.

中文翻译：

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IL-20通过激活PKC / NADPH氧化酶途径来上调氧化应激，从而促进缺氧/复氧诱导的线粒体功能障碍和心肌细胞凋亡。

急性心肌梗塞（AMI）是最大的严重心血管事件，在全球范围内导致高发病率和高死亡率。AMI中发生的缺血和再灌注会导致心肌细胞凋亡和细胞功能异常。IL-20是IL-10的家族成员，参与多种炎症性疾病。因此，我们试图阐明IL-20在缺血/再灌注（I / R）损伤后梗死的心脏中的作用。我们发现在H2C2心肌母细胞和接受低氧/复氧（H / R）刺激的心室组织中，IL-20及其受体IL-20R1和IL-20R2增加。IL-20的存在进一步抑制了H9C2细胞和原代心肌细胞的细胞活力。我们的结果表明，IL-20引起Ca2 +的增加和PKC / NADPH氧化酶途径的激活，导致氧化酶压力升高和AKT下调。此外，我们证明IL-20能够通过PKC / NADPH氧化酶/ AKT信号介导H / R诱导的细胞凋亡。我们的发现表明，IL-20在体外和遭受I / R损伤的大鼠心脏中对H / R应激有反应，并且IL-20的这种上调可能有助于心肌细胞的凋亡。