PDF(Pubmed)
Abstract：
Background and Objectives: Selenium deficiency represents a risk factor for the occurrence of severe diseases, such as acute kidney injury (AKI). Recently, selenoprotein-p1 (SEPP1), a selenium transporter, mainly released by the liver, has emerged as a promising plasmatic biomarker of AKI as a consequence of cardio-surgery operations. The aim of the present study was to investigate, on an in vitro model of hypoxia induced in renal tubular cells, HK-2, the effects of sodium selenite (Na2SeO3) and to evaluate the expression of SEPP1 as a marker of injury. Materials and Methods: HK-2 cells were pre-incubated with 100 nM Na2SeO3 for 24 h, and then, treated for 24 h with CoCl2 (500 µM), a chemical hypoxia inducer. The results were derived from an ROS assay, MTT, and Western blot analysis. Results: The pre-treatment determined an increase in cells\' viability and a reduction in reactive oxygen species (ROS), as shown by MTT and the ROS assay. Moreover, by Western blot an increase in SEPP1 expression was observed after hypoxic injury as after adding sodium selenite. Conclusions: Our preliminary results shed light on the possible role of selenium supplementation as a means to prevent oxidative damage and to increase SEPP1 after acute kidney injury. In our in vitro model, SEPP1 emerges as a promising biomarker of kidney injury, although further studies in vivo are necessary to validate our findings.
摘要：
背景与目的:硒缺乏是严重疾病发生的危险因素,如急性肾损伤（AKI）。最近,硒蛋白-p1（SEPP1），硒转运蛋白,主要由肝脏释放，作为心脏手术的结果，已成为AKI的有希望的血浆生物标志物。本研究的目的是调查，在肾小管细胞缺氧诱导的体外模型上，HK-2、亚硒酸钠(Na2SeO3)的影响并评价SEPP1的表达作为损伤标记物。材料和方法：将HK-2细胞与100nMNa2SeO3预孵育24小时，然后,用CoCl2（500µM）处理24小时，化学缺氧诱导剂。结果来自ROS测定，MTT,和蛋白质印迹分析。结果：预处理确定了细胞活力的增加和活性氧（ROS）的减少，如MTT和ROS测定所示。此外，通过Westernblot，在低氧损伤后与添加亚硒酸钠后一样，观察到SEPP1表达增加。结论：我们的初步结果揭示了补充硒作为预防急性肾损伤后氧化损伤和增加SEPP1的手段的可能作用。在我们的体外模型中，SEPP1作为肾损伤的一个有希望的生物标志物，尽管需要进一步的体内研究来验证我们的发现。
