Glucocorticoid Receptor Agonist Dexamethasone Attenuates Renal Ischemia/Reperfusion Injury by Up-regulating eNOS/iNOS

The aim of this study was to determine the effect of dexamethasone(DEX) on renal ischemia/reperfusion injury(IRI). C57BL/6 mice were randomly divided into Sham group, IRI group and DEX group. The mice in IRI and DEX groups subjected to renal ischemia for 60 min, were treated with saline or DEX(4 mg/...

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Published in:Journal of Huazhong University of Science and Technology. Medical sciences Vol. 34; no. 4; pp. 516 - 520
Main Author: 张炯 李俊华 王艻 韩敏 肖芳 兰小勤 李月强 徐钢 姚颖
Format: Journal Article
Language:English
Published: Heidelberg Huazhong University of Science and Technology 01-08-2014
Department of Nephrology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China
Department of Nephrology, Subsidiary of the Sichuan Academy of Sciences & Sichuan Provincial People's Hospital, University of Electronic Science and Technology, Chengdu 610072, China%Department of Nephrology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China%Department of Gastroenterology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China
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Summary:The aim of this study was to determine the effect of dexamethasone(DEX) on renal ischemia/reperfusion injury(IRI). C57BL/6 mice were randomly divided into Sham group, IRI group and DEX group. The mice in IRI and DEX groups subjected to renal ischemia for 60 min, were treated with saline or DEX(4 mg/kg, i.p.) 60 min prior to I/R. After 24 h of reperfusion, the renal function, renal pathological changes, activation of extracellular signal-regulated kinase(ERK) and glucocorticoid receptor(GR), and the levels of iNOS and eNOS were detected. The results showed DEX significantly decreased the damage to renal function and pathological changes after renal IRI. Pre-treatment with DEX reduced ERK activation and down-regulated the level of iNOS, whereas up-regulated the level of eNOS after renal IRI. DEX could further promote the activation of GR. These findings indicated GR activation confers preconditioning-like protection against acute IRI partially by up-regulating the ratio of eNOS/iNOS.
Bibliography:ischemia/reperfusion injury; dexamethasone; nitric oxide synthase
The aim of this study was to determine the effect of dexamethasone(DEX) on renal ischemia/reperfusion injury(IRI). C57BL/6 mice were randomly divided into Sham group, IRI group and DEX group. The mice in IRI and DEX groups subjected to renal ischemia for 60 min, were treated with saline or DEX(4 mg/kg, i.p.) 60 min prior to I/R. After 24 h of reperfusion, the renal function, renal pathological changes, activation of extracellular signal-regulated kinase(ERK) and glucocorticoid receptor(GR), and the levels of iNOS and eNOS were detected. The results showed DEX significantly decreased the damage to renal function and pathological changes after renal IRI. Pre-treatment with DEX reduced ERK activation and down-regulated the level of iNOS, whereas up-regulated the level of eNOS after renal IRI. DEX could further promote the activation of GR. These findings indicated GR activation confers preconditioning-like protection against acute IRI partially by up-regulating the ratio of eNOS/iNOS.
42-1679/R
ISSN:1672-0733
1993-1352
DOI:10.1007/s11596-014-1308-y