Protective Effects And Mechanisms Of Extract Of Astragalus On Global Cerebral Ischemia-reperfusion Injury

Extract of astragalus (EA) is effective components of astragalus which is mainly composed of astragalosides and astragalus polysaccharides. Effects of EA on acute cerebral ischemia or anoxia in mice and global cerebral ischemia-reperfusion in rats were studied in this paper. Besides we also investigated probable mechanisms of its neuroprotective effects. The main results are showed as follows:1 Effects of EA on acute cerebral ischemia or anoxia in miceOn anoxia under normal pressure model, EA(50,100 mg kg-1) could significantly prolong the survival time of anoxic mice. And EA(50,100 mg kg-1) also prolonged the gasping time of mice after quick decapitation. In mice subjected to acute cerebral ischemia induced by bilateral common carotid artery occlusion, EA(50,100 mg kg-1) could prolong the survival time and EA(100 mg kg-1) significantly decreased the death rate during 12 hours after ischemia.2 Effects of E A on global cerebral ischemia and 24h reperfusion in ratsThis experiment was performed to evaluate effects of EA on acute neuronal injury induced by four vessels occlusion (4VO) for 20min and reperfusion for 24h in rats. During reperfusion after ischemia, EA(40,80 mg kg-1) significantly promoted the recovery of inhibited electroencephalogram and righting reflex. EA(20,40,80 mg kg-1) could reduce the brain edema obviously and lessen histopathological alterations of cortex in brain sections. SOD, GSH-Px and LDH activities increased in brain homogenate of rats treated by EA(20,40,80 mg kg-1) and MDA content decreased treated by EA(40,80 mg kg-1). EA(20,40,80 mg kg-1) might inhibit total NOS activityin brain homogenate. Simultaneously EA(40,80mg kg-1) reduced iNOS immunoreactivity in brain sections. ET content was estimated by radio-immunoassay both in plasma and hippocampal homogenate. EA(40,80 mg kg-1) could markedly inhibit the increase of ET content after ischemia and reperfusion. 3 Effects of EA on global cerebral ischemia and 7d reperfusion in ratsThis experiment was performed to evaluate effects of EA on delayed neuronal injury induced by four vessels occlusion for 10min and reperfusion for 7d in rats. EA(20,40mg kg-1) could ameliorate the ischemic histopathological changes in hippocampus of brain tissue staining by hematoxylin and eosin. Meanwhile, EA(20,40 mg kg-1) lessened neuronal ultrastructural alterations in hippocampus induced by ischemia and reperfusion observed by electron microscope. EA(20,40,80 mg kg-1) inhibited the profound enhancement of GFAP immunoreactivity in hippocampus CAl sector submit to ischemia and reperfusion.Conclusion: EA took protective effects during acute cerebral ischemia or anoxia in mice and global cerebral ischemia and reperfusion in rats. The role of anti-oxidation, inhibiting formation of iNOS and ET, decreasing GFAP expression might contribute to its neuroprotective effects.