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Effect of bcl-xl overexpression in transgene mice with cerebral infarction and study of cytochrome C expression and caspase-3 expression
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- Author:
- No author available
- Journal Title:
- CHINESE JOURNAL OF EMERGENCY MEDICINE
- Issue:
- 9
- DOI:
- 10.3760/j.issn:1671-0282.2007.09.007
- Key Word:
- 转基因小鼠;脑梗死;bcl-xl基因;细胞色素C;Caspase-3
Abstract： 目的 观察大脑中动脉栓塞模型转基因小鼠中bcl-xl的过表达对脑缺血后再灌流的保护作用及其机制.方法 建立bcl-xl过表达转基因小鼠模型,将该模型小鼠与同种系野生型小鼠同时行线栓永久性阻塞大脑中动脉,在缺血24 h时测其神经功能评分,观察转基因小鼠与野生型小鼠的差别.在缺血后不同时间点分别检测两种小鼠梗死体积及其动态变化、脑组织中bcl-xl的表达量的差异、再灌流时凋亡细胞的数量和分布情况以及脑中细胞色素C及caspase-3的表达量及分布情况.结果 转基因小鼠的神经功能评分低于野生型小鼠.在缺血后不同时间点,转基因小鼠的梗死体积小于并且皮质缺血区内的凋亡细胞数明显少于野生型小鼠,且保护作用发生时间早,持续时间较长.梗死前后转基因小鼠的皮质细胞bcl-xl的表达量均明显高于野生型小鼠,且梗死后两种小鼠体内的ocl-xl的表达量均有所增加,但两者之间差异无统计学意义(P＞0.05).缺血后再灌流后不同时间点,转基因小鼠缺血局部细胞色素C的表达及caspase-3的活化明显低于野生型小鼠.结论 在规范化的标准条件下,转基因小鼠中bcl-xl基因的过表达能够降低脑梗死的体积并改善小鼠的神经功能.过表达bcl-xl基因的这种效应可能是通过抑制细胞凋亡而实现的,其机制可能是bcl-xl基因的过表达抑制了细胞色素C的释放及caspase-3的活化.
- [1]王芙蓉,袁慧,肖文伍,等.人bcl-xl转基因小鼠外源基因的复制及传代的稳定性观察[J].2002,(6).
- [2]肖文伍,王芙蓉,张苏明,等.用显微注射法建立转bcl-x1基因小鼠[J].2002,(3).
- [3]王芙蓉,姜永生,肖文伍,等.颈内动脉线栓法建立小鼠局灶性脑缺血再灌注模型[J].2003,(2).
- [4]Parsadanian, A. S.,Cheng, Y.,Keller-Peck, C. R.,etc.Bcl-x~L is an Antiapoptotic Regulator for Postnatal CNS Neurons[J].1998,18(3).
- [5]Lee SH,Lee YS,Son H,etc.Co-transfection with cDNA encoding the Bcl family of anti-apoptotic proteins improves the efficiency of transfection in primary fetal neural stem cells.[J].2002,117(2).
- [6]Hashimoto Nobuo,Miyatake ShinIchi,Ishii Kazuhiro,etc.Overexpression of basic fibroblast growth factor and Bcl-xL with adenoviral vectors protects primarily cultured neurons against glutamate insult.[J].2002,50(4).
- [7]Wiessner C,Hesselbarth D,Mies G,etc.A reproducible model of middle cerebral artery occlusion in mice: hemodynamic, biochemical, and magnetic resonance imaging.[J].1998,18(4).
- [8]Colbourne F,Iadecola C,Li H,etc.Caspase inhibitors reduce neuronal injury after focal but not global cerebral ischemia in rats.[J].2000,31(1).
- [9]Xuesong Liu,Hua Zou,Clive Slaughter,etc.DFF, a Heterodimeric Protein That Functions Downstream of Caspase-3 to Trigger DNA Fragmentation during Apoptosis[J].1997,89(2).
- [10]Sommer C,Kiessling M.Ischemia and ischemic tolerance induction differentially regulate protein expression of GluR1, GluR2, and AMPA receptor binding protein in the gerbil hippocampus: GluR2 (GluR-B) reduction does not predict neuronal death.[J].2002,33(4).
- [11]Pinsky DJ,Winfree CJ,Solomon RA,etc.Procedural and strain-related variables significantly affect outcome in a murine model of focal cerebral ischemia.[J].1996,38(3).
- [12]Bischoff S,Rupalla K,Allegrini PR,etc.Neuron-specific transgene expression of Bcl-XL but not Bcl-2 genes reduced lesion size after permanent middle cerebral artery occlusion in mice.[J].1999,268(3).