To investigate the effect of miR-10a on renal tissues with ischemia reperfusion (I/R) injury in rats and to explore the underlying mechanisms of the effect of miR-10a on hypoxia–reoxygenation in HK-2 cells. MiR-10a level was measured in the renal tissues of rats with I/R rats using RT-PCR. In order to research the role of miR-10a in renal tissues, an miR-10 agonist and an miR-10a antagonist were used to treat I/R-injured rats. Levels of serum creatinine and blood urea nitrogen, renal histopathology, and levels of cell apoptosis were analyzed separately in renal tissues from the rats. Phosphatidylinositol 3-kinase (PI3K)/Akt pathway related proteins were measured by Western blotting. In addition, HK-2 cells were cultured in order to study the mechanism of action of miR-10a in the hypoxia-reoxygenation model being studied. Finally, the dual luciferase reporter gene assay was used to confirm that the PI3K p100 catalytic subunit α (PIK3CA) gene was targeted by miR-10a. After renal I/R injury in rats, miR-10a expression increased significantly (p < 0.05). Injection of miR-10a agonist significantly aggravated the renal injury and raised the level of cell apoptosis in the renal tissues of I/R-injured rats (p < 0.05). However, administration of miR-10a antagonist led to obvious improvement of the renal injury, decreased renal cell apoptosis, and inhibited PI3K/Akt pathway activity (p < 0.05). In in vitro experiments, the negative relationship between PIK3CA and miR-10a levels was confirmed. Furthermore, overexpression of miR-10a significantly decreased the proliferation of HK-2 cells, and increased cell apoptosis via up-regulation of the PI3K/Akt pathway (p < 0.05). The aggravation of renal I/R injury by miR-10a was associated with a decrease in the activity of PIK3CA/PI3K/Akt pathway.

中文翻译：

---

miR-10a 过表达加重与 PIK3CA 表达降低相关的肾缺血再灌注损伤。

研究miR-10a对大鼠缺血再灌注（I/R）损伤肾组织的影响，并探讨miR-10a对HK-2细胞缺氧-复氧作用的潜在机制。使用 RT-PCR 测量 I/R 大鼠肾组织中的 MiR-10a 水平。为了研究 miR-10a 在肾组织中的作用，使用 miR-10 激动剂和 miR-10a 拮抗剂治疗 I/R 损伤大鼠。在大鼠肾组织中分别分析血清肌酐和血尿素氮水平、肾脏组织病理学和细胞凋亡水平。通过蛋白质印迹法测量磷脂酰肌醇 3-激酶 (PI3K)/Akt 途径相关蛋白。此外，培养HK-2细胞以研究miR-10a在所研究的缺氧-复氧模型中的作用机制。最后，双荧光素酶报告基因检测用于确认 PI3K p100 催化亚基 α (PIK3CA) 基因被 miR-10a 靶向。大鼠肾 I/R 损伤后，miR-10a 表达显着增加（p < 0.05）。注射miR-10a激动剂显着加重了I/R损伤大鼠肾组织的肾损伤并提高了细胞凋亡水平（p < 0.05）。然而，给予 miR-10a 拮抗剂导致肾损伤明显改善，肾细胞凋亡减少，并抑制 PI3K/Akt 通路活性（p < 0.05）。在体外实验中，证实了 PIK3CA 和 miR-10a 水平之间的负相关关系。此外，miR-10a 的过表达显着降低了 HK-2 细胞的增殖，并通过上调 PI3K/Akt 途径增加了细胞凋亡（p < 0.05）。