Effects of dexamethasone on Fas/Fas ligand expression and apoptosis of hepatocytes in rats with LPS-induced acute liver injury

AIM: To investigate the changes of expression of hepatocytes apoptosis and Fas/Fas ligand (FasL) in lipopolysaccharide (LPS) induced acute liver injury in rats and the effects of treatment by dexamethasone and to evaluate the potential role and mechanism in the pathogenesis of acute liver injury. METHODS: Expression of Fas/FasL protein and mRNA was detected using immunohistochemistry and in situ hybridization, respectively. Apoptosis was determined by terminal UTP nick end labelling (TUNEL) in rats during every phase of acute liver injury. RESULTS: Expression of Fas/FasL protein and mRNA was upregulated and correlated with the increased apoptosis in hepatocytes of rats with lipopolysaccharide (LPS) induced acute liver injury ( P 0.05). The administration of dexamethasone suppressed apoptosis as well as expression of Fas/FasL protein and mRNA ( P 0.05). CONCLUSION: Dysregulation of apoptosis and activation of Fas/FasL system may play a key role in the pathogenesis of LPS induced acute liver injury in rats, which worsens the early stage acute liver injury. The protective effects of dexamethasone may obstruct the activation of Fas/FasL system and apoptosis of hepatocytes in rats with LPS induced acute liver injury and thus alleviate liver damage.