Thirty-seven Glycol Pretreatment Induced Brain Ischemic Tolerance And GFAP And IL-1 �� MRNA Expression Level

Objective:To investigate the influence of Panasadiol Saponins(PDS) preconditioning on the cerebral ischemia in rats and the probable mechanisms,we set up a focal cerebral ischemia model and observe the changes of nerve function, Nissl body,infarct volume,the expression of Glial fibriUary acidic protein(GFAP) and interleukin-1β(IL-1β)mRNA in brain after acute cerebral ischemia.Method:SD rats randomly divided into six groups:blank,model(NS+ MCAO),ischemic preconditioning(IPC+MCAO),PDS preconditioning(PDS+M CAO),PDS treatment(MCAO+PDS),sham operated(SS+SS).Nonintervention to blank group;after intraperitoneal injection of NS continuously 3 days to mode 1 group,gave 2h MCAO,executed after reperfusion 22h;10 min IPC to IPC group,3 days later,gave 2h MCAO,executed after reperfusion 22h;10min SS to SS group,gave 2h SS after 3 days,executed after 24h;PDS for 3 days t o PDS+MCAO group,gave 2h MCAO,executed after model building 24h.2h MCAO to MCAO+PDS group,executed after PDS treatment for 3 days;obser ving the information of loss of nerve function of rats after model building,pat hological changes of HE dyeing,Nissl body observation of Nissl dyeing,inf arct volume detection of TTC dyeing,observation of GFAP masculine expressi on of immunity tissue chemistry dyeing,detection of IL-1βmRNA express lev el of RT-PCR.Experimental data was dealt with SPSS13.0,tested statistic with ONE-WAY ANOVA.Result:cerebral infarction volume of IPC+MCAO and PDS+MCAO group are more decreased than MCAO group,there are statistic differences among the three groups(p＜0.05),the IOD of nissl body and GFAP express levels of IPC+MCAO and PDS+MCAO group are higher than MCAO group,there are statistic differences among the three groups(p＜0.05).IL-1βmRNA express levels of IPC+MCAO and PDS+MCAO group are decreased compare with MCAO group,there are statistic differences among the three groups(p＜0.05). Conclusion:PDS preconditioning may intluce ischemic toleranee in organism, and protects against neuronal damages after subsequent lethal ischemic insults.The activation of Astrocytes and inhibit inflammatory reaction are possibly the important mechanism of PDS preconditioning induced ischemic tolerance.