The Effect of Dexamethasone on Expression of Inducible Nitric Oxide Synthase Gene During Liver Warm Ischemia-reperfusion in Rat

Background: Liver ischemia / reperfusion Injury (IRI) is one of the major causes of liver failure during various types of liver surgery, trauma and infections. The present study investigates the effect of dexsamethasone on the liver injury and inducible nitric oxide synthase gene expression during hepatic warm ischemia/reperfusion in rats. Materials and Methods: 24 male Wistar rats (200-250 g) were randomly divided into 3 group 8 rat each: 1) saline treated group (Control), 2) saline - administered ischemia/reperfusion insulted group (IR), and 3) dexamethasone - administered IR group (DEX + IR). Dexamethasone were injected twice at a dose of 8 mg/kg intraperitoneally (60 min before ischemia and immediately after reperfusion). After 1 h of ischemia and 3 hours of subsequent reperfusion, blood and liver samples were collected. Results: Ischemia significantly increases serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels in the IR group which significantly were reduced by dexamethasone in DEX + IR group (P< 0.05). In parallel to this finding, according to histopathological imaging, dexamethasone reduces hepatic tissue damages. In addition elevated inducible nitric oxide synthase gene expression in IR was significantly decreased in DEX + IR group (P< 0.05). Conclusion: Dexamethasone, an anti- imflammatory drug, can decline hepatic IR stimulated damages through inhibition of immune mediated reactions and inhibition of iNOS gene expression.