AIM Oxidative stress plays an important role in myocardial ischemia-reperfusion injury. Pleckstrin homology-like domain, family A, member 1 (PHLDA1) was first identified in apoptosis induced by T cell receptor activation, and was shown to play a different role in different cell types and under different stimuli. The role and mechanism of PHLDA1 in oxidative stress-induced cardiomyocyte injury and cardiac ischemia-reperfusion were therefore determined. MAIN METHODS Cell viability and apoptotic rate were measured by Cell Counting Kit-8 and flow cytometry, respectively. Mitochondrial membrane potential was measured using JC-1 test kit. Reactive oxygen species (ROS) production was detected using ROS kit. HE staining was used to detect histological morphology, 2,3,5-triphenyltetrazolium chloride staining to detect infarct size, terminal deoxynucleotidyl transferase dUTP nick end labeling staining to detect the apoptotic rate, and immunohistochemistry and western blot analysis to detect protein expression. The binding of PHLDA1 to Bcl-2 associated X (Bax) was detected by immunoprecipitation. KEY FINDINGS The results indicated that PHLDA1 is highly expressed in oxidative stress-induced cardiomyocyte and myocardial ischemia-reperfusion injuries. PHLDA1 overexpression in cardiomyocytes promoted oxidative stress-induced cardiomyocyte injury. At the same time, PHLDA1 knockdown improved oxidative stress-induced cardiomyocyte and myocardial ischemia-reperfusion injuries. In addition, PHLDA1 binds to Bax and the interaction is enhanced under H2O2 stimulation. SIGNIFICANCE The present results indicated that PHLDA1 interacts with Bax to participate in oxidative stress-induced cardiomyocyte injury and myocardial ischemia reperfusion injury.

中文翻译：

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PHLDA1是氧化应激和局部缺血再灌注引起的心肌损伤的新治疗靶标。

目的氧化应激在心肌缺血-再灌注损伤中起重要作用。Pleckstrin同源样域，家族A，成员1（PHLDA1）首先在T细胞受体激活诱导的细胞凋亡中被鉴定，并显示在不同的细胞类型和不同的刺激下起不同的作用。因此确定了PHLDA1在氧化应激诱导的心肌细胞损伤和心肌缺血-再灌注中的作用和机制。主要方法分别通过Cell Counting Kit-8和流式细胞仪测量细胞活力和凋亡率。线粒体膜电位使用JC-1测试试剂盒进行测量。使用ROS试剂盒检测了活性氧（ROS）的产生。HE染色用于检测组织学形态，2,3,5-三苯基四唑氯化物染色用于检测梗塞面积，末端脱氧核苷酸转移酶dUTP缺口末端标记染色可检测细胞凋亡率，免疫组织化学和蛋白质印迹分析可检测蛋白质表达。通过免疫沉淀检测PHLDA1与Bcl-2相关X（Bax）的结合。主要研究结果表明，PHLDA1在氧化应激诱导的心肌细胞和心肌缺血再灌注损伤中高表达。PHLDA1在心肌细胞中的过表达促进了氧化应激诱导的心肌细胞损伤。同时，PHLDA1组合可改善氧化应激诱导的心肌细胞和心肌缺血-再灌注损伤。此外，PHLDA1与Bax结合，并且在H2O2刺激下相互作用增强。