Kidney ischemia–reperfusion injury is a common pathophysiological phenomenon in the clinic. A large number of studies have found that the tyrosine protein kinase/signal transducer and activator of transcription (JAK/STAT) pathway is involved in the development of a variety of kidney diseases and renal protection associated with multiple drugs. Edaravone (EDA) is an effective free radical scavenger that has been used clinically for the treatment of postischemic neuronal injury. This study aimed to identify whether EDA improved kidney function in rats with ischemia–reperfusion injury by regulating the JAK/STAT pathway and clarify the underlying mechanism. Histomorphological analysis was used to assess pathological kidney injury, and mitochondrial damage was observed by transmission electron microscopy. Terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) staining was performed to detect tubular epithelial cell apoptosis. The expression of JAK2, P-JAK2, STAT3, P-STAT3, STAT1, P-STAT1, BAX and Bcl-2 was assessed by western blotting. Mitochondrial function in the kidney was assessed by mitochondrial membrane potential (ΔΨm) measurement. The results showed that EDA inhibited the expression of p-JAK2, p-STAT3 and p-STAT1, accompanied by downregulation of the expression of Bax and caspase-3, and significantly ameliorated kidney damage caused by ischemia–reperfusion injury (IRI). Furthermore, the JC-1 dye assay showed that edaravone attenuated ischemia–reperfusion-induced loss of kidney ΔΨm. Our findings indicate that EDA protects against kidney damage caused by ischemia–reperfusion through JAK/STAT signaling, inhibiting apoptosis and improving mitochondrial injury.

中文翻译：

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依达拉奉通过JAK / STAT途径减轻缺血再灌注所致肾脏损伤中的细胞凋亡和线粒体损伤。

肾脏缺血再灌注损伤是临床中常见的病理生理现象。大量研究发现，酪氨酸蛋白激酶/信号转导子和转录激活子（JAK / STAT）通路参与多种肾脏疾病的发展以及与多种药物相关的肾脏保护。依达拉奉（EDA）是一种有效的自由基清除剂，已在临床上用于治疗缺血性神经元损伤。这项研究旨在通过调节JAK / STAT通路并阐明其潜在机制，来确定EDA是否能改善缺血再灌注损伤大鼠的肾功能。组织形态学分析用于评估病理性肾脏损伤，并通过透射电子显微镜观察线粒体损伤。进行末端脱氧核苷酸转移酶介导的dUTP缺口末端标记（TUNEL）染色以检测肾小管上皮细胞凋亡。通过蛋白质印迹法评估JAK2，P-JAK2，STAT3，P-STAT3，STAT1，P-STAT1，BAX和Bcl-2的表达。肾脏中的线粒体功能通过线粒体膜电位（ΔΨm）测量进行评估。结果表明，EDA抑制p-JAK2，p-STAT3和p-STAT1的表达，同时下调Bax和caspase-3的表达，并显着改善缺血再灌注损伤（IRI）对肾脏的损害。此外，JC-1染料分析表明依达拉奉减轻了缺血再灌注引起的肾脏Δm损失。我们的研究结果表明，EDA可通过JAK / STAT信号转导防止缺血再灌注引起的肾脏损害，