A Preliminary Study of Dexamethasone Against Ischemia/Reperfusion Liver Injury in Rats

The hepatoprotective effect of dexamethasone was investigated in rats exposed to ischemia/reperfusion liver injury. Ischemia was induced by clamping the pedicle of the left hepatic lobe for I h followed by 3 h of reperfusion. Dexamethasone was administered 24 h before the ischemic insult in two i.p., doses (10 mg kg(-1), each) with 12 h interval. Dexamethasone significantly attenuated the ischemia/reperfusion-induced elevations in serum aminotransferase and hepatic levels of tumor necrosis factor-a and nitric oxide. Dexamethasone also significantly compensated deficits in hepatic antioxidant defense mechanisms (reduced glutathione and catalase and superoxide dismutase activities) and suppressed lipid peroxidation observed with liver hypoxia-reoxygenation. This was associated with significant restoration of the ischemia/reperfusion-induced increase in hepatic caspase-3 activity. Neutrophil infiltration and hepatocellular necrosis and apoptosis detected by histopathological examination of liver tissue were markedly ameliorated by pre-ischemic dexamethasone treatment. In conclusion, dexamethasone can be considered a potential therapeutic agent to protect against the major clinical challenge of liver injury resulting from ischemia/reperfusion.