Effect Of Ulinastatin On The Expression Of Bcl-2、Fas、Caspase-3 In The Cortex Of Cerebral Ischemia Reperfusion Rats

Objective: To explore the effect of ulinastatin on the expression of Bcl-2, Fas and Caspase-3proteins and protective cerebral mechanism after cerebral ischemia-reperfusion, toprovide theory for clinical application.Methods: Middle cerebral artery occlusion (MCAO) and the model of reperfusionfollowingfocal cerebral ischemia were made using an intraluminal filament method.Twenty-four Wistar rats were selected and randomized into four groups: shamgroup (A group), ischemia- reperfusion group(B group), the high dose of ulinastatintreated group (C group) and the low dose of ulinastatin treated group (D group),each group involve six rats. The rats of B group can be injected 1ml salineimmediately after the model, the rats of C group and D group could be injectedimmediately the ulinastatin at the 10000U/kg dose and 50000U/kg doserespectively , once every 12 hours and up to death. The changes of pathology wereobserved by light microscope. The expression of Bcl-2, Fas and Caspase-3 proteinswere detected using the combinal analysis of immune-histochemical and the ImageAnalysis System .Results: 1.The naked eye: Groups on both sides of the brain volume are similar, the samecolor and brain structure, section is pale grey, yellow and soft. The microscope: Agroup list a basic normal cortical structures, cell clarity of outline, neurons are moreabundant cytoplasm; at high magnification, it has the rounded and big nucleus,there is one or two clear nucleoli.2.Immunohistochemistry results: Compared with the A group ,the expression ofBcl-2,Fas,Caspase-3 proteins in B、C and D groups are increased, and thecomparative differences are statistically significant (both P<0.05). Compared withthe B groups, the expression of Bcl–2 were significantly increased in C and Dgroups, while the expression of Fas and Caspase-3 proteins in C and D groups weresignificantly lower than those in the B group (both P <0.05). The expression levelof the Bcl-2 in D group were high than in C group, the expression of Fas andCaspase-3 in D group significantly decreased as compared with C group,(bothP<0.05), the comparative differences are statistically significant.Conclusion:1.Ulinastatin can inhibit cerebral neuron apoptosis in ischemia-reperfusion injury.2. Its anti-apoptotic mechanism may raise the expression of Bcl-2 protein and inhibitthe expression of Fas protein and Caspase-3 protein. 3.Protective effects of ulinastatin is on the cerebral dose-dependent, high-dose effectis not obvious, and may be associated with the doses are too small.