巴曲酶对沙土鼠前脑缺血再灌注损伤后神经元凋亡的时间效应关系研究

目的：研究巴曲酶对沙土鼠前脑缺血冉灌注损伤后海马CA1区神经元凋亡的影响及时间效应关系，探讨其可能的作用机制。方法：采用双侧颈总动脉夹闭5min后再通建立沙土鼠前脑缺血再灌注的损伤模型，在不同时间点腹腔注射巴曲酶（8BU／kg）对其进行治疗，运州未端脱氧核仔酸转移酶介导的dUTP-生物素切口末端标记法（TUNEL）及免疫组织化学方法，检测沙土鼠海马CA1区神经元中的TUNEL染色阳性细胞数及凋广相关基因Bcl-2、Bax免疫反应阳性细胞数。结果：治疗组TUNEL染色阳性细胞数明显减少，与对照组之间差异有显著性（P〈0．05）；与对照组相比，治疗组海马CA1区Bcl-2表达明显增加，Bax表达降低．尤以缺血再灌注前6h、即刻、缺血再灌注后1、3及6h最明显（P〈0．01）。结论：巴曲酶可减少脑缺血再灌注后神经细胞的凋亡．发挥脑保护作用．其作用存在明显时效关系．机制可能是增强Bcl-2的表达及抑制Bax的表达有关。

Relationship between time and effect of Batroxobin on apoptosis after cerebral ischemia/reperfusion in gerbils

Objective: To discuss the effect and possible mechanism of relationship between time and effect of Batroxobin onapoptosis after cerebral ischemia/reperfusion in gerbils. Methods: Gerbils were treated with Batroxobin (8 BU/kg) injection throughabdominal at different time before and after cerebral ischemia/reperfusion (I/R). Terminal deoxynucleotidyltransferasemediated dUTP-biotin nick end labeling (TUNEL) was performed to dectect the apoptosis cells. The expressions of Bcl-2 and Bax in neuron ofhippocampal CA1 region were detected through immunohistochemistry method. Results: Positive cells were seen in all slices ofcerebral ischemia/reperfusion gerbils. The number of positive cells declined by using Batroxobin compared with control groups.Compared with the control group, the expression of Bcl-2 in hippocampal CA1 region increased obviously while the expression of Baxdecreased in treated group, The best effects were seen at the range from 3 hours before I/R to 6 hours after I/R. Conclusion:Batroxobin injection may reduce the apoptosis of neuron after I/R through enhancing the expression of Bcl-2 and inhibiting theexpression of Bax. The effect of Batroxobin injection on cerebral I/R was time dependent.