Mongolian Medicine Heisuga-25 Reperfusion In Acute Cerebral Ischemia Mechanism Of Injury Protection

Objective:To explore the mechanism of Mongolian Heisuga-25 on acute cerebral ischemia and reperfusion injury,and to provide a basis for Mongolian Heisuga-25 for clinical treatment of ischemic stroke.Methods:In this experimental study,50 SPF grade SD male rats were randomized by body weight into sham,model,Kinado positive,Heisuga-25 high and low-dose group,10 in each group.In the high-and low-dose groups of Heisuga-25,Heisuga-25-25 0.64g/kg,0.16g/kg was given respectively,and the Jinnado-positive group was given 16.8mg/kg,20ml/kg volume,the sham surgery group and model group were given isovolume saline,1 time / d for 7d.The right rat middle cerebral artery occlusion model was prepared 7d after drug administration,and after 90 min of ischemia,the wire plug was withdrawn for reperfusion.In the sham group,only the right common carotid artery was exposed.After 90 min of ischemia and 24 h of reperfusion,Zealonga nerve deficit score,the size of cerebral infarction were analyzed by HE staining,ELISA,and Bcl-2 gene expression by PCR.Results:(1)Zealonga Neurological deficit score: Zealonga Neurological deficit score: intra-group comparison: 24 h after reperfusion,the model group-25 rats was higher than 90 min,with statistical difference(P <0.05);the model group was the most significant(P <0.01).Comparison between groups: 24 h after reperfusion,the neurological deficit score increased significantly in the model group compared with the Jinnardo positive group and the Heisuga-25 high dose group,with significant statistical difference(P <0.01).(2)The volume was detected by TTC staining: The volume of cerebral infarction in the Jinnardo positive group and the Heisuga-25 high and low dose(P <0.05);the Jinnardo positive group compared with the Heisuga-25 high dose group(P <0.05).(3)HE staining: In the model group,the number of neurons and glial cells decreased,the cell morphology disappeared,the nuclear sequestration and fragmentation were loose,and the brain pathology of the Heisuga-25 was less severe than that in the model group,and the Heisuga-25.(4)SOD,MDA,and NSE levels in serum by ELISA: Compared with the model group,the SOD levels in the Jinnardo-positive group and the Heisuga-25 high and low-dose group increased(P <0.01);compared with the Jinnardo-positive group(P <0.05).Compared with the model group,MDA and NSE levels were significantly lower in the Jinnardo positive group,Heisuga-25 high and low dose groups with significant statistical difference(P<0.01);serum MDA and NSE levels in the Jinnardo Heisuga-25 high dose group showed significant statistical difference(P <0.01).(5)Gene expression of Bax and Bcl-2 was detected by PCR: Compared with the model group,the relative expression of Bax in the Jinnardo-positive,Heisuga-25 high and low-dose rats was significantly reduced(P <0.01).Compared with the model group,the relative expression of Bcl-2 in the Jinnardo positive,Heisuga-25 high and low dose rats was significantly increased in the brain tissue(P <0.01).Conclusion:The Mongolian Heisuga-25 can improve the cerebral ischemia reperfusion injury model rat serum SOD level,reduce MDA and NSE levels,and downregulate Bax gene expression,upregulate Bcl-2 gene expression to reduce the oxidative stress response of cerebral ischemia reperfusion injury and inhibit apoptosis,to improve the nerve dysfunction after cerebral ischemia reperfusion injury,reduce the volume of cerebral infarction,reduce neuronal cell damage,protection against acute cerebral ischemia reperfusion injury.