The Molecular Mechanism Of 灯盏花乙素 Viscapine Against Cerebral Ischemia - Reperfusion Injury In Rats

Objective To explore the role of peroxynitrite(ONOOˉ) and Poly-(ADP-ribose) polymerase(PARP) in cerebral ischemia and reperfusion(I/R) injure and the molecular mechanism of Scutellarin against cerebral I/R injury, in rats. Methods Using rat model of cerebral I/R injury in rat.Adult male Sprague-Dawley were randomly assigned to the follow groups:sham operation group ; modelⅠgroup (NS) ; modelⅡgroup (DW) ; normal rats+Scutellarin:Scutellarin (100mg/kg,i.p.); model+Scutellarin:Scutellarin(100mg/kg,i.p.);model+PARPinhibitor(3-aminobe-nzamide,10mg/kg,i.p.).Each group has 8 SD rats.The dynamoic alterations of expression of nitrotyrosine (NT),which was produced by ONOOˉand labeled with NT immunohistochemistry in frontal and parietal cortex in rat brains were investigated after the middle cerebral artery occlusion (MCAO). Results The expression of NT reached its peak value at 12h in cerebral I/R injury. NT antigen positive products were observed in modelⅠgroup and modelⅡgroup, not in sham operation group. Compared with those in sham-operated group ,the activity of MPO in brain tissues increased markedly in modelⅠgroup and modelⅡgroup.From the rough shape, the modelⅠgroup and modelⅡgroup become obvious edemia,disordered cell,nuclear contracted. Nissle Body decreased and dinered,perikaryon disvolved and be small,loss of normal structure.Compared with those in modelⅠgroup and modelⅡgroup, NT antigen products and the activity of MPO decreased in model + Scutellarin Group and model +3-aminobenzamide group(P<0．01) .Among model + Scutellarin Group and model + 3-aminobenzamide group, the cerebral I/R injury was relieved. No NT antigen positive products were seen in normal rats+灯盏花乙素group. The activity of MPO and cerebral I/R injury did not change significantly in normal rats+ Scutel larin group.Conclusion ONOOˉand PARP may play a role in the injury of I/R neuron. The molecular mechanism of灯盏花乙素viscapine against cerebral I/R injury in rats might be related to ONOOˉ-PARP pathway.