The Study Of The Infarction Size And The Expression Of BDNF In Rat Injected Plasmid PLXSN-mediated Transfer Of Bcl-2 Gene By Intraventricular

prefacecerebralvascular disease ( C VD ) has been one of the three major disease endangered human healthy, and its'prognosis is badness. So CVD& treatment and diagnosis become the emphases of study. Now gene treatment is one of the developed methods. It s the Gene treatment which adopt the effective carrier, for example plasmid, virus and so on , to lead to cerebral vessel , ventricle and organize all round . to express the material which be fit to blood vessel growth ,or anti - apoptosis , or prevent more harmness. It is the treatment of ischemic CVD protected penumbra from the more damage, and the fusion of the cell death in penumbra is apoptosis . so anti - apoptosis is the major treat way. It has been demonstrated Bcl - 2 is the important anti - apoptosis gene, we used the plasmid pLXSN - mediated transfer Bcl - 2 gene to treat ischemic CVD by intraventricular in rat.Methods135 wistar rat were randomly assigned in 3 groups ( Bcl - 2 treated group, saline group and pLXSN group ) , there were 45 rats in every group. And we studied the infarct volumes , Bcl - 2 and BDNF ( Brain Derived Neurotrophic Factor) expression in 3,6,24,48,72hours after MCAO(middle cerebral occlusion) , Temporary ischemia of the MCA for 2 hours was induced by the suture occlusion technique, after MCAO we injected 20 ul plasmid pLXSN - mediated transfer Bcl - 2 gene by intraventricular.Resultthe infarction volume of the treaty group are significantly less than the control group in 24h, 48h, 72h after MCAO(p <0.05). however, there arent different between three groups in 3h and 6h after MCAO(p >0.05). the expression of Bcl -2 and BDNF are significantly increased in treaty group in 24h,48h and 72h after MCA0( p < 0. 01) ; in 3h and 6h after MCAO, the expression of Bcl -2 and BDNF are same between treaty group and control group(p >0.05).Discussion: our study find Bcl - 2 gene can protect the ischemic neuron, decrease the infarction size and markedness increase the expression of Bcl - 2 and BDNF in cortex . the study showed the expression of Bcl - 2 gene is not increase in every time between the saline group and the pLXSN group, in 3,6 hour after MCAO the treaty group hasnt increased, but significantly increase in 24, 48,72 hour compared the control group. Moreover the peak time is at 24 hour , it is not same with the 6hour peak time in previous study, our study showed that the plasmid pLXSN - mediated transfer Bcl - 2 gene can increase the expression of Bcl - 2 and BDNF, delay the time of the expression to exert the anti - apopto-sis function.We furthermore observed the effect on infarction size by Bcl -2. the result showed there are not same between the saline group and the pLXSN group, it demonstrated pLXSN has not side - effect, and not treaty effect. The infarction size isnt decrease in 3 ,6 hour, is significantly decrease in 24,48,72 hour in Bcl - 2 treatment group than the control group. It approved Bcl - 2 injection by intraventricular can protect the cerebral organize from ischemic damage.Conclusionour study demonstrated Bcl - 2 can decrease cerebral infarct size and increase expression of BDNF by intraventricular injection . one possible mechanism of action of Bcl -2 after temporary ischemia appears to be the neuroprotection of up - regulated BDNF.