Abstract Context: Reperfusion injury after myocardial infarction is associated with inflammation response and oxidative stress. Aim: The aim of our study is to explore the influence of suppressor of ras val-2 (SRV2) on cardiomyocyte oxidative stress and inflammation response under hypoxia-reoxygenation (HR) injury. Methods: Cell viability was determined via MTT assay. qPCR and western blots were used to analyze the alterations of SRV2 and mammalian STE20-like protein kinases 1 (Mst1). ELISA and qPCR were used to verify the alterations of antioxidants and pro-inflammatory factors. Results: SRV2 was upregulated by HR injury in cardiomyocyte. Interestingly, loss of SRV2 attenuated HR injury-mediated cardiomyocyte damage through inhibiting cardiomyocyte apoptosis. At the molecular levels, SRV2 deletion reduced inflammation and oxidative stress induced by HR injury and thus promoted cardiomyocyte survival. Besides, SRV2 deletion inactivated the Mst1-mROS signaling pathway in cardiomyocyte and thus regulated the inflammation and oxidative stress. Interestingly, overexpression of Mst1 abolished the beneficial effects exerted by SRV2 deletion on HR-mediated cardiomyocyte death. Conclusions: SRV2 upregulation, induced by reperfusion injury, contributes to cardiomyocyte death through the Mst1-mROS signaling pathway.

中文翻译：

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ras val-2抑制剂通过激活Mst1-mROS信号通路促进心肌细胞炎症介导的氧化应激和细胞凋亡

摘要背景：心肌梗死后的再灌注损伤与炎症反应和氧化应激有关。目的：我们研究的目的是探讨ras val-2（SRV2）抑制因子对缺氧-复氧（HR）损伤下心肌细胞氧化应激和炎症反应的影响。方法：通过MTT法测定细胞活力。qPCR 和蛋白质印迹用于分析 SRV2 和哺乳动物 STE20 样蛋白激酶 1 (Mst1) 的改变。ELISA 和 qPCR 用于验证抗氧化剂和促炎因子的变化。结果：心肌细胞HR损伤导致SRV2上调。有趣的是，SRV2 的缺失通过抑制心肌细胞凋亡减轻了 HR 损伤介导的心肌细胞损伤。在分子水平上，SRV2 缺失减少了由 HR 损伤引起的炎症和氧化应激，从而促进了心肌细胞的存活。此外，SRV2缺失使心肌细胞中的Mst1-mROS信号通路失活，从而调节炎症和氧化应激。有趣的是，Mst1 的过表达消除了 SRV2 缺失对 HR 介导的心肌细胞死亡的有益影响。结论：再灌注损伤诱导的 SRV2 上调通过 Mst1-mROS 信号通路导致心肌细胞死亡。