CAJ | 학술논문

目的研究大鼠全脑缺血再灌注后海马区细胞凋亡情况及尼莫地平处理的影响.方法选取成年雄性Wistar大鼠54只.实验动物随机分为假手术组、盐水对照组、药物治疗组.假手术组只进行手术操作,不结扎双侧颈动脉.盐水对照组和药物治疗组采用四条血管阻断方法制备全脑缺血再灌注模型后,分别于0、6、12、24?h时间点开始并累积腹腔注射生理盐水[5ml/(kg·次)]和尼莫地平(1mg/kg).用流式细胞仪检测海马区细胞凋亡率及Bax、Bcl-2基因的表达情况.结果 (1) 缺血再灌注后盐水对照组海马区凋亡细胞比假手术组明显增多,差异具有非常显著性(P<0.01).(2) 缺血再灌注后,药物治疗组海马区凋亡细胞明显比盐水对照组少,差异具有非常显著性(P<0.01);0、6?h细胞凋亡率小于12、24?h,差异具有显著性(P<0.05).(3) 药物治疗组Bcl-2蛋白的表达量大于盐水对照组,而Bax则小于盐水对照组,差异具有显著性(P<0.05).结论尼莫地平可明显抑制脑缺血再灌注损伤后神经细胞凋亡,其抗凋亡作用可能与增加Bcl-2表达有关,早期用药作用显著.
목적 연구대서전뇌결혈재관주후해마구세포조망정황급니막지평처리적영향.방법 선취성년웅성Wistar대서54지.실험동물수궤분위가수술조、염수대조조、약물치료조.가수술조지진행수술조작,불결찰쌍측경동맥.염수대조조화약물치료조채용사조혈관조단방법 제비전뇌결혈재관주모형후,분별우0、6、12、24?h시간점개시병루적복강주사생리염수[5ml/(kg·차)]화니막지평(1mg/kg).용류식세포의검측해마구세포조망솔급Bax、Bcl-2기인적표체정황.결과 (1) 결혈재관주후염수대조조해마구조망세포비가수술조명현증다,차이구유비상현저성(P<0.01).(2) 결혈재관주후,약물치료조해마구조망세포명현비염수대조조소,차이구유비상현저성(P<0.01);0、6?h세포조망솔소우12、24?h,차이구유현저성(P<0.05).(3) 약물치료조Bcl-2단백적표체량대우염수대조조,이Bax칙소우염수대조조,차이구유현저성(P<0.05).결론 니막지평가명현억제뇌결혈재관주손상후신경세포조망,기항조망작용가능여증가Bcl-2표체유관,조기용약작용현저.
Objective To observe the protective effect of Nimodipine on the neurons of rats with global cerebral ischemia-reperfusion injury.Methods All rats were divided into three groups at random:sham-operated group,control group and treated group.Four-vessel occlusion was used to establish the model of global cerebral ischemia-reperfusion in the control group and treated group.The normal saline and Nimodipine was injected intraperitoneally in control groups and treated groups at 0?h,6?h,12?h,24?h after reperfusion respectively.The flow cytometry was used to determine cellular apoptosis rate and expression of Bcl-2、Bax protein.Results (1) The cellular apoptosis rate of hippocampal region in control group was higher than that in sham-operated group (P<0.01) and treated group (P<0.01).The cellular apoptosis rate was increased at 0?h and 6?h than 12?h and 24?h in treated group (P<0.05).The expression of Bcl-2 in treated group was higher than that in control group,while the expression of Bax in treated group was lower than that in control group.Conclusion Nimodipine could effectively reduce apoptosis after global cerebral ischemia-reperfusion injury.The mechanism of effects of Nimodipine would be related with increasing expression of Bcl-2.The effect would be better if useing it in earlier time-spot.