【摘要】 目的　研究质粒 pLXSN介导bcl 2基因在局灶性脑缺血中的脑保护作用。 方法　 5 4只雄性大鼠随机分为生理盐水组、空质粒组和bcl 2组 ,每组 18只。分别于皮质区两部位注射生理盐水、质粒 pLXSN、pLXSN bcl 2 ,并于注射后 2 4h采用改良线栓法制备大鼠大脑中动脉缺血 2 4h模型。采用TTC染色、免疫组织化学方法、原位细胞凋亡检测、流式细胞仪检测各组大鼠脑梗死状况、bcl 2蛋白表达和细胞凋亡。结果　 (1)标尺测量各组注射点 1、2处及两者中点处冠状轴上脑梗死内缘距大脑纵裂距离 ,生理盐水组分别为 (2 70± 0 36 )mm、(2 5 2± 0 2 7)mm、(2 33± 0 16 )mm ;空质粒组分别为 (2 83± 0 4 7)mm、(2 5 9± 0 6 7)mm、(2 6 3± 0 38)mm ;bcl 2组分别为 (4 2 2± 0 80 )mm、(4 77± 0 74 )mm、(3 5 7± 1 4 9)mm。于注射点 1、2处 ,与生理盐水组和空质粒组比较 ,bcl 2组的脑梗死内缘距中线距离显著增大 (P <0 0 1) ;于两注射点中点处脑梗死内缘距中线距离 3组差异无显著意义。 (2 )显微图像分析系统、免疫组化检测注射处缺血半暗带bcl 2阳性细胞面积百分比 ,生理盐水组为 0 93%± 0 2 6 %、空质粒组为 0 95 %± 0 37%、bcl 2组为 1 95 %± 0 6 5 % ,与前两组比较 ,bcl 2组注射处缺血半暗更多还原

【Abstract】 Objective To observe the neuroprotection of plasmid pLXSN-mediated transfer of bcl-2 gene during focal cerebral ischemia.Methods 54 male Wistar rats were randomly divided into three groups: normal saline(NS) control group, plasmid control group, and bcl-2 group.NS, plasmid-pLXSN and plasmid-pLXSN-bcl-2 were respectively injected into two sites in the rat cerebral cortex 24 hours before induction of neocortical focal ischemia by occlusion of the right middle cerebral artery for 24 hours.The condition of local ischemic damage, expression of bcl-2 and the apoptosis in neural cells were confirmed respectively by staining with 2% 2,3,5-triphenyltetrazolium chloride, immunohistochemistry, in site cell apoptosis detection and flow cytometry. Results In the injection sites 1, 2 and midpoint, the extent of viable tissue from the longitudinal fissure to the medial edge of the infarction were measured with a surveyor’s rod.It is respectively (2.70±0.36)mm,(2.52±0.27)mm,(2.33±0.16)mm in NS control group; (2.83±0.47)mm,(2.59±0.67)mm,(2.63±0.38)mm in plasmid control group and (4.22±0.80)mm,(4.77±0.74)mm,(3.57±1.49)mm in bcl-2 group.In injection sites viable tissue of the bcl-2 group was significantly increased (P<0.01).The expression of bcl-2 in bcl-2 group (1.9517%±0.6522%) than those in NS control group (0.9306%±0.2611%) or in plasmid control group (0.9527%±0.3674%)was significantly increased (P<0.01).The apoptosis in neural cells in bcl-2 group (38.35±3.02) than those in the NS control group (61.67±13.55) or in the plasmid control group (58.33±15.25) was significantly reduced (P<0.01 or P<0.05).Conclusion Plasmid pLXSN-mediated transfer of bcl-2 gene may inhibit apoptosis of neurol cells resulting in neuroprotection during focal cerebral ischemia.更多还原