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促红细胞生成素δ可降低原代人肾小管细胞中的氧化应激。

Epoetin delta reduces oxidative stress in primary human renal tubular cells.

作者信息

De Beuf Annelies, Hou Xiang-hua, D'Haese Patrick C, Verhulst Anja

机构信息

Laboratory of Pathophysiology, Faculties of Medicine and Biomedical, Pharmaceutical and Veterinary Sciences, University of Antwerp, Universiteitsplein 1, 2610 Antwerp, Belgium.

出版信息

J Biomed Biotechnol. 2010;2010:395785. doi: 10.1155/2010/395785. Epub 2010 May 5.

DOI:10.1155/2010/395785
PMID:20454536
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2864893/
Abstract

Erythropoietin (EPO) exerts (renal) tissue protective effects. Since it is unclear whether this is a direct effect of EPO on the kidney or not, we investigated whether EPO is able to protect human renal tubular epithelial cells (hTECs) from oxidative stress and if so which pathways are involved. EPO (epoetin delta) could protect hTECs against oxidative stress by a dose-dependent inhibition of reactive oxygen species formation. This protective effect is possibly related to the membranous expression of the EPO receptor (EPOR) since our data point to the membranous EPOR expression as a prerequisite for this protective effect. Oxidative stress reduction went along with the upregulation of renoprotective genes. Whilst three of these, heme oxygenase-1 (HO-1), aquaporin-1 (AQP-1), and B-cell CLL/lymphoma 2 (Bcl-2) have already been associated with EPO-induced renoprotection, this study for the first time suggests carboxypeptidase M (CPM), dipeptidyl peptidase IV (DPPIV), and cytoglobin (Cygb) to play a role in this process.

摘要

促红细胞生成素（EPO）具有（肾脏）组织保护作用。由于尚不清楚这是否是EPO对肾脏的直接作用，我们研究了EPO是否能够保护人肾小管上皮细胞（hTECs）免受氧化应激影响，若能保护，涉及哪些途径。EPO（δ-促红细胞生成素）可通过剂量依赖性抑制活性氧生成来保护hTECs免受氧化应激。这种保护作用可能与EPO受体（EPOR）的膜表达有关，因为我们的数据表明膜EPOR表达是这种保护作用的前提条件。氧化应激的减轻与肾保护基因的上调同时出现。虽然其中三种基因，即血红素加氧酶-1（HO-1）、水通道蛋白-1（AQP-1）和B细胞淋巴瘤/白血病-2（Bcl-2）已经与EPO诱导的肾保护作用相关，但本研究首次表明羧肽酶M（CPM）、二肽基肽酶IV（DPPIV）和细胞珠蛋白（Cygb）在这一过程中发挥作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a54c/2864893/0dee7582d63d/JBB2010-395785.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a54c/2864893/c7a24782ac03/JBB2010-395785.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a54c/2864893/ff43be83a914/JBB2010-395785.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a54c/2864893/4fba35b437db/JBB2010-395785.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a54c/2864893/2549c1ee9a4e/JBB2010-395785.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a54c/2864893/b78406a4846a/JBB2010-395785.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a54c/2864893/0dee7582d63d/JBB2010-395785.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a54c/2864893/c7a24782ac03/JBB2010-395785.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a54c/2864893/ff43be83a914/JBB2010-395785.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a54c/2864893/4fba35b437db/JBB2010-395785.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a54c/2864893/2549c1ee9a4e/JBB2010-395785.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a54c/2864893/b78406a4846a/JBB2010-395785.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a54c/2864893/0dee7582d63d/JBB2010-395785.006.jpg

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