| The form of neuronal cell death is apoptosis besides infarction at the time of cerebral ischemic - reperfusion damage. And apoptosis plays an important role. Apoptosis is a kind of cell death which is mediated by gene. Bcl-2 gene is the major gene to resist the apoptosis. When bcl-2 gene is transferred to brain, its expression in cells is increased and the neuronal cell apoptosis is decreased or inhibited. The neuronal cells are protected. At the same time, the adhesion of leucocyte and endothelial cell plays an important role at the time of ischemic -reperfusion damage. ICAM-1 is a key mediator which enhances the adhesion of leucocyte and endothelial cells. The expression of ICAM-1 is up regulated when brain is ischemic which can increase the adhesion of leucocyte and endothelium cells and result in the damage of cerebral ischemic - reperfusion. This study implies it is helpful to decrease the damage of reperfusion to increase the expression of bcl-2 and decrease the expression of ICAM - 1. We used the model of cerebral middle artery ischemic - reperfusion in rats. After injecting bcl-2 gene of pLXSN-mediated transfer into lateral ventricle, we observe the volume of cerebral infarction and the expression of bcl-2 and ICAM-1 to prove the protection of bcl-2 to neuronal cells and discuss the relation between bcl-2 and ICAM - 1.Material and Method135 healthy Wistar rats Weighed 250 - 300g were randomized into three groups: NS group, plasmid group, bcl-2 group. There are 45 rats in every group. Five time points, of reperfusion at 3,6,24,48,72 hours after ischemic for 2 hours were divided into five sub groups, which 9 rats in each. MCAO mod-el was made by line way and rats were immediately put on the brain localizing machine. The lateral ventricle was injected NS, plasmid plXSN, pLXSN-bcl-2 by the localizing technique. Reperfusion was made when MCAO had been done successfully in rats. 5 rats were taken cut from every sub group and cut the heads and harvested the brains at the time of ischemic - reperfusion (3h,6h, 24h,48h,72h) ,stained by TTC. The volume of infarction was accumulated and measured by micro picture analyzing system. 4 rats in every sub group were reperfused and heads were harvested after 3,6,24,48,72h of ischemic - reperfusion. They were stabilized and made into sections. Bcl-2 and ICAM-1 were stained by immunohistochemistry and accumulated; analyzed by the system. The expression of bcl-2 and ICAM-1 were observed. The data were expressed by x ?s. T test was made to analysis the difference in groups, (p <0. 05 has a statistical means. )Results1. The volume of infarction; Every time point has no difference in NS groups than in plasmid group( p > 0.05). 3h and 6h are the same in bcl-2 group than in plasmid group ( 3h: 54. 89 1. 06 VS 56. 25 1. 69, 6h: 134. 82 54. 92 VS 134. 82 20. 78, p >0. 05). The volume of infarction was decreased obviously at 24,48,72hours( 24h: 89. 19 11. 87 VS 234. 27 10. 01, 48h: 131.41 12.02 VS 212.12 21.78, 72h:70. 64 9.21 VS 133.71 20.13 , p<0.05).2. Expression of bcl-2 protein: The expressions are the same at each time point in NS group than in plasmid group ( p > 0. 05 ). The expression of bcl-2 was increased obviously in bcl-2 group compared with plasmid group ( 3h: 98.07 1.68 VS 85. 261.67, 6h: 101. 14 3. 84 VS 87. 83 2.13, 24h: 97.18 2.23 VS 85.981.02, 48h: 100. 63 3.21 VS 88.73 0.96, 72h 99.45 2.12 VS 87.31 0.89, p<0.05).3. Expression of ICAM-1 protein; The expression at every time point is the same in NS group than in plasmid group (p >0. 05). The expression of ICAM-1 at 3h is the same in bcl-2 group than in plasmid group( 87.22 3. 86 VS 89.952.26, p >0.05), The expression of ICAM-1 at 6,24,48,72 hours was less in bcl-2 group than in plasmid group ( 6h: 75. 88 1.26 VS 90. 06 2.44, 24h: 73.75 1.48 VS 89.62 2.08, 48h: 72.76 2. 88 VS 89. 25 2.17, 72h: 76.41 1.90 VS91.54 1.42, p<0.05).DiscussionResearch has proved that the main form of neuronal cell death is apoptosis after cerebral ischemic - reperfusion...
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