Glucocorticoid receptor agonist dexamethasone attenuates renal ischemia/reperfusion injury by up-regulating eNOS/iNOS.
10.1007/s11596-014-1308-y
- Author:
Jiong ZHANG
1
;
Jun-hua LI
;
Le WANG
;
Min HAN
;
Fang XIAO
;
Xiao-qin LAN
;
Yue-qiang LI
;
Gang XU
;
Ying YAO
Author Information
1. Department of Nephrology, Huazhong University of Science and Technology, Wuhan, 430030, China, zhangjiong831224@163.com.
- Publication Type:Journal Article
- MeSH:
Animals;
Dexamethasone;
pharmacology;
Gene Expression Regulation, Enzymologic;
drug effects;
Glucocorticoids;
pharmacology;
Male;
Mice;
Nitric Oxide Synthase Type II;
biosynthesis;
Nitric Oxide Synthase Type III;
biosynthesis;
Receptors, Glucocorticoid;
agonists;
Reperfusion Injury;
enzymology;
pathology;
Up-Regulation;
drug effects
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2014;34(4):516-520
- CountryChina
- Language:English
-
Abstract:
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.
