Introduction: Ulinastatin, a trpsin inhibitor, has been reported that can inhibits the liver inflammation and improves the liver function. The role of UTI on liver warm ischemia reperfusion injury (IRI) and the underlying mechanisms remain to be further investigated.

Materials and Methods: In bred C57BL/6 mice and liver warm IRI model were employed. The ligamentum of hepatoduodenale was clamped for 45 mins and followed with reperfusion of 1 hour, 6 and 24 hours, respectively. UTI was treated preoperatively. Serum enzyme release, liver cell histology and apoptosis, and Caspase-3 mRNA & Fas mRNA expression from the liver tissues were examined, respectively.

Results: ALT/AST levels were remarkably lower in UTItreated group than IRI control group at reperfusion time of 1hour, 6 and 24 hours.Liverhistological examine showed that hepatic cells edema，degeneration, vacuolization, some patchy necrosis, and sinusoidal congestion were obviously in the IRI control group at 6 hours reperfusion, While UTI treatment reduced the liver tissue damage significantly. The expression of Caspase-3 mRNA and Fas mRNA were detected significantly higher in IRI control group than that in UTI treated group（P<0.05）. The production of IL-6 and TNF-α were elevated in the IRI control group and suppressed by UTI treatment (P<0.05). Moreover, the apoptotic activate of liver cells in the IRI+UTI group was reduced significantly than that in IRI control group.

Conclusion: Ulinastatin treatment prevents liver IRI significantly. The underlying mechanisms of the protective role of UTI on liver IRI may through inhibition of proinflammatory cytokines IL-6 and TNF-α, down-regulation of pro-appoptotic genes Caspase-3 mRNA and Fas mRNA expression，and prevention of liver cells from apoptotic death.