| Objective: To investigate the potential protective effects of ulinastatin of apoptosis on cerebralischemia-reperfusion injury in rats and analyze the possible mechanism.Mechods: 24 heathly male Wistar rats were randomly divided into 4 groups, n=6: sham group,model group, UTI 10000U/kg treatment group, UTI 50000U/kg treatment group. The models ofthe focal cerebral rats were made by the middle cerebral artery occlusion except sham group.After ischemia for 1h and reperfusion for 24h, the expression of caspase-3,bcl-2,bax by themethod of immunohistochemistry and apoptosis by TUNEL were detected. The pathologicalfeature of cerebral tissue was detected by HE staining. SPSS13.0 version was used forstatistical analysis and P<0.05 was regared as statistical significance.Results: After 1h and 24h reperfusion, compared with the sham group ,the number of apoptoticcells in the brain tissue in the model group was significantly increased(P<0.01). In the modelgroup, the expression of caspase-3 and bax was increased (P<0.01),and bcl-2 was decreasedcompared with sham group(P<0.01); Ulinastatin groups can reduced the number of apoptoticcells in brain(P<0.01) and reduced the expression of caspase-3,bax (P<0.01), increased bcl-2protein expression (P<0.05,P<0.01). The ischemia-reperfusion injury in brain tissuepathological in Ulinastatin groups changes was lighter than model group.Conclusion: Ulinastatin has a protective effect on cerebral ischemia-reperfusion injury bydecreasing the protein expression of caspase-3, bax and increasing protein expression of bcl-2in brain tissues to reduce the apoptosis of brain cells.
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