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

• Published in: Journal of Huazhong University of Science and Technology. Medical sciences 2014-08, Vol.34 (4), p.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: Article
• Language: English
• Subjects: Animals; Dexamethasone - pharmacology; eNOS; Gene Expression Regulation, Enzymologic - drug effects; Glucocorticoids - pharmacology; iNOS; Male; Medicine; Medicine & Public Health; Mice; Nitric Oxide Synthase Type II - biosynthesis; Nitric Oxide Synthase Type III - biosynthesis; Receptors, Glucocorticoid - agonists; Reperfusion Injury - enzymology; Reperfusion Injury - pathology; Up-Regulation - drug effects; 再灌注损伤; 受体激动剂; 地塞米松; 糖皮质激素受体; 细胞外信号调节激酶; 缺血; 肾功能
• ISSN: 1672-0733; 1993-1352
• DOI: 10.1007/s11596-014-1308-y

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.