AIM:To study the effect of
buflomedil on polymorphonuclear leukocytes(PMNs) in filtration after cerebral ischemia reperfusion
injury on rats. METHODS:The experiment was completed in the Cerebrovascular Laboratory,the Dep artment of Neurology,the First Affiliated Hospital of Zhengzhou University.Total ly 144 healthy male SD rats were divided into sham operated group,operated grou p,physiological saline
treatment group and
buflomedil chlorhydrate treatment gro up at random,36 rats in each group.Rat transient cerebral ischemic injury model was established with suture emboli method.In operated group, rats were sacrifice d at 1,3,6,12,24,48 hours respectively after 1 hour of middle cerebral arter y occlusion(MCAO),the brains were taken out, sliced and embedded in paraffin use d to examine nuclear factor kappa B65(NF κB65), intercellular adhesion molec ule 1(ICAM 1),macrophage inflammation protein 1α(MIP 1α)and myeloperoxidas e(MPO) with immunohistochemical method.Then computer image analysis system was u sed to analyze the gray values of NF κB65,ICAM 1,MIP 1αand MPO,and the path ological observation was performed. RESULTS: Activated NF κB65,ICAM 1,MIP 1αand MPO immunoreactive cells wer e observed at each time point in the operated group,physiological saline treatme nt group and buflomedil chlorhydrate treatment group but not in sham operated g roup.There were no significant differences in the gray values of NF κB65,ICAM 1,MIP 1αand MPO between the operated group and physiological saline treatmen t group(P >0.05).The gray values of NF κB65,ICAM 1,MIP 1αand MPO were highe r in the buflomedil chlorhydrate treatment groups than in the operated groups an d physiological saline treatment group operated groups,except for the 1 hour re perfusion group(NF κb65:100.13±3.31;ICAM 1:153.90±3.82;MIP 1α:187.72±3.4 1 )(P< 0.05). CONCLUSION:The cerebral protection of buflomedil chlorhydrate can carry out by reducing PMN infiltration against inflammation.