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.
Subject(s)
Animals , Male , Mice , Dexamethasone , Pharmacology , Gene Expression Regulation, Enzymologic , Glucocorticoids , Pharmacology , Nitric Oxide Synthase Type II , Nitric Oxide Synthase Type III , Receptors, Glucocorticoid , Reperfusion Injury , Pathology , Up-RegulationABSTRACT
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.
ABSTRACT
Objective To discuss the pathogenesis,diagnosis and treatment of delayed traumatic intracerebral hematoma.Methods The clinic data of traumatic delayed intracranial hematoma patients in this hospital were retro- spectively analyzed.According to clinic observation and CT re-examination,47 cases were diagnosed as delayed trau- matic intracranial hematoma(45 cases by operative treatment,and the other 2 by conservative treatment).Results There were 21 cases of recovery,10 cases of slight disability,8 cases of severe disability,8 cases of death.The total mortality rate was 17 %.Conclusion Brain contusion,subarachnoid hemorrhage and skull base fracture were impor- tant factors of DTICH.Fine-observation and prompt CT re-examination offered excellent results for DTICH.