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促红细胞生成素可防止高糖环境下活性氧的产生和肾小管细胞凋亡。

Erythropoietin prevents reactive oxygen species generation and renal tubular cell apoptosis at high glucose level.

机构信息

Department of Nephrology, Renmin Hospital, Wuhan University, 99, Ziyang Road, Wuhan 430060, China.

出版信息

Biomed Pharmacother. 2010 Dec;64(10):681-5. doi: 10.1016/j.biopha.2010.06.011. Epub 2010 Jul 16.

Abstract

Erythropoietin (EPO) can induce a series of cytoprotective effects in many non-hematopoietic tissues through interaction with the erythropoietin receptor (EPOR), but whether EPO can prevent the overproduction of reactive oxygen species (ROS) and apoptosis in diabetes remains unclear. Here, we report that renal tubular cells possess EPOR and that EPO reduces high glucose-induced oxidative stress in renal tubular cells. Further, we found that EPO inhibited high glucose-induced renal tubular cell apoptosis and that this protective effect was dependent on reduction of Bax/caspase-3 expression as well as elevation of Bcl-2 expression. Our results suggest that EPO can inhibit high glucose-induced renal tubular cell apoptosis through direct effect on anti-oxidative stress and that EPOR may play a key role in this process.

摘要

促红细胞生成素(EPO)通过与促红细胞生成素受体(EPOR)相互作用,可在许多非造血组织中诱导一系列细胞保护作用,但 EPO 是否能防止糖尿病中活性氧(ROS)的过度产生和细胞凋亡尚不清楚。在这里,我们报告说肾小管细胞具有 EPOR,EPO 可降低高葡萄糖诱导的肾小管细胞氧化应激。此外,我们发现 EPO 抑制高葡萄糖诱导的肾小管细胞凋亡,这种保护作用依赖于 Bax/caspase-3 表达的减少和 Bcl-2 表达的增加。我们的结果表明,EPO 可以通过直接的抗氧化应激作用抑制高葡萄糖诱导的肾小管细胞凋亡,而 EPOR 可能在这个过程中发挥关键作用。

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