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目的研究B细胞白血病/淋巴瘤-2原癌基因(Bcl-2)和发状分裂相关增强子-1(Hes1)在脑缺血预处理后介导的神经保护作用。方法模型A组,以大脑中动脉闭塞法建立脑缺血模型;模型B组,行右侧颈内动脉短暂性血流阻断10 min 1次,3 d后,同模型A方法建立缺血模型;假手术组,大鼠仅需分离颈总动脉。于术后2,3,7,14 d,通过Zea-Longa法评估各组大鼠的神经行为,2,3,5-三苯基氯化四氮唑(TTC)染色法检测脑梗死体积,实时荧光定量聚合酶链式反应(qRT-PCR)法测定Bcl-2和Hes1 mRNA水平。结果与模型A组比较,模型B组的各时间点神经功能缺损评分都明显降低(P<0.05),模型A与B组的脑梗死体积分别为(40.00±4.47)%,(19.00±2.75)%,A组显著大于B组(P<0.05)。模型A、B组Hes1 mRNA的表达均高于假手术组(P<0.05),但模型B组明显高于模型A组(均P<0.05)。Bcl-2 mRNA的表达,与假手术组比较,模型B组再灌注2 d时表达明显增高,且明显高于模型A组(P<0.05)。结论脑缺血预处理后Bcl-2和Hes1 mRNA的表达较脑缺血组增高,可能与神经保护效应相关。
Objective To study the neuroprotective effects of Bcl-2 / Bm-2 and Hes1 after cerebral ischemic preconditioning. Methods In model group A, cerebral ischemia model was established by occlusion of middle cerebral artery. In model group B, transient occlusion of right internal carotid artery was blocked for 10 min for 1 time. After 3 days, ischemic model In the sham group, only the common carotid artery was separated in rats. At 2, 3, 7 and 14 days after operation, the neurological behaviors of rats in each group were evaluated by Zea-Longa method, the infarct volume was measured by 2,3,5-triphenyltetrazolium tetrazolium (TTC) Real-time fluorescent quantitative polymerase chain reaction (qRT-PCR) was used to determine the mRNA levels of Bcl-2 and Hes1. Results Compared with model group A, the score of neurological deficit in model group B at each time point was significantly lower (P <0.05), and the volume of cerebral infarction in model group A and group B were (40.00 ± 4.47)% and (19.00 ± 2.75) %, A group was significantly greater than B group (P <0.05). The expression of Hes1 mRNA in model group A and group B was higher than that in sham operation group (P <0.05), but the model group B was significantly higher than model group A (all P <0.05). Compared with the sham group, the expression of Bcl-2 mRNA in model group B was significantly increased 2 d after reperfusion, which was significantly higher than that in model group A (P <0.05). Conclusions The expression of Bcl-2 and Hes1 mRNA in cerebral ischemic preconditioning is higher than that in cerebral ischemic group, which may be related to neuroprotective effect.