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GSE was administered in a dose of 50 mg\/kg\/day orally for 15 days before I\/R injury and repeated before the reperfusion period. Liver samples were taken for histological examination or determination of hepatic malondialdehyde (MDA), glutathione (GSH) and myeloperoxidase (MPO) activity. Serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels were determined to assess liver functions. Lactate dehydrogenase (LDH) and cytokines (TNF\u2010<jats:italic>\u03b1<\/jats:italic> and IL\u20101<jats:italic>\u03b2<\/jats:italic>) were also assayed in serum samples for the evaluation of generalized tissue damage. Ischemia\/reperfusion caused a significant decrease in hepatic GSH, and significant increases in MDA level, and MPO activity. Serum AST and ALT levels, as well as LDH activity and plasma TNF\u2010<jats:italic>\u03b1<\/jats:italic> and IL\u20101<jats:italic>\u03b2<\/jats:italic> levels were also elevated in the I\/R group. Treatment with GSE reversed all these biochemical parameters as well as histological alterations induced by I\/R. In conclusion, GSE reduced I\/R\u2010induced organ injury through its ability to balance the oxidant\u2013antioxidant status, to inhibit neutrophil infiltration and to regulate the release of inflammatory mediators. 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