Dexamethasone protects from renal ischemia/reperfusion injury: a possible association with SGK-1
| Autor: | Agnes Prokai, K Meszaros, C Juanxing, Attila J. Szabo, Uwe Heemann, Jens Lutz, Tivadar Tulassay, K Pásti, Krisztina Rusai, Veronika Müller, Balázs Szalay |
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| Rok vydání: | 2013 |
| Předmět: |
musculoskeletal diseases
Male Programmed cell death medicine.medical_specialty Pathology Ischemia Renal function Protein Serine-Threonine Kinases Dexamethasone Cell Line Immediate-Early Proteins Western blot In vivo Physiology (medical) Internal medicine Medicine Animals Humans Phosphorylation Glucocorticoids medicine.diagnostic_test business.industry General Medicine Hypoxia (medical) Acute Kidney Injury musculoskeletal system medicine.disease In vitro Endocrinology Reperfusion Injury medicine.symptom business medicine.drug |
| Zdroj: | Acta physiologica Hungarica. 100(2) |
| ISSN: | 0231-424X |
| Popis: | Previous experimental data suggest that steroids might have protective effects during hypoxic/ischemic injury of various organs. In this study, the association between dexamethason (Dexa) treatment and the anti-apoptotic SGK-1 was tested in ischemic renal injury. In vitro, HK-2 cells were exposed to 24 h hypoxia, and the effect of Dexa incubation on SGK-1 expression / activation and on cell death was studied. In an in vivo rat model of unilateral renal IR, animals were treated with Dexa, and serum renal function parameters, tissue injury and SGK-1 expression and localization were examined after different reperfusion times (2 h, 4 h and 24 h). Dexa at a dose of 2 mg/L exerted a protective effect on cell survival assessed by LDH release and vital staining paralleled by marked up-regulation of SGK-1. In rats, 2 mg/kg Dexa treatment 24 h prior to ischemia resulted in less severe tissue injury and ameliorated urea nitrogen levels 24 h after reperfusion. Furthermore, SGK-1 expression and phosphorylation were higher in Dexa animals demonstrated by Western blot and immunofluorescence technique. Our results provide novel data on the signalling mechanism of Dexa under hypoxia / ischemia and further support that Dexa emerges as an attractive pharmacological agent for the prevention of ischemic injury. |
| Databáze: | OpenAIRE |
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