Abstract: Carbon tetrachloride (CCl4) is a well known model compound for inducing hepatic injury in experimental animals. The aim of this study was to evaluate the hepatoprotective potential of a somatostatin analogue (octreotide 30 μg kg-1) in mice following oral administration of carbon tetrachloride (CCl4, 0.5 mL kg-1). Hepatic total thiol was determined colorimetrically by Elman’s reagent. Expression levels of somatostatin receptor-2 and vascular endothelial growth factor were detected by immunoblotting using specific antibodies against SSTR-2 and VEGF. Administration of CCl4 caused a significant increase in the release of serum Alanine Aminotransferase (ALT), Aspartate Aminotransferase (AST) and total bilirubin. Significantly enhanced hepatic lipid peroxidation and marked depletion of reduced glutathione were observed after CCl4 intoxication. It was also found that CCl4 Administration caused over expression of TNF-α mRNA and Vascular Endothelial Growth Factor (VEGF) protein. Octreotide treatment showed hepatic protection by significantly reducing elevated levels of AST and ALT enzymetic activities, lipid peroxidation and total bilirubin which had been raised by acute intoxication of CCl4 in addition to its ability to increase total thiol. Notably, octreotide significantly reduced expression of the inflammatory marker tumor necrosis factor alpha (TNF-α) mRNA and VEGF protein. Moreover, octreotide treatment was accompanied by marked increase in the expression of somatostatin receptor type-2 (SSTR2). The results of this study indicate that octreotide has potential protective effects against liver injury.