摘要
目的:研究巴曲酶对沙土鼠前脑缺血再灌注损伤后海马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,运用末端脱氧核苷酸转移酶介导的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亡相关基因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。
Objective： To discuss the effect and possible mechanism of relationship between time and effect of Batroxobin on apoptosis after cerebral ischemia/reperfusion in gerbils. Methods： Gerbils were treated with Batroxobin （8 BU/kg） injection through abdominal at different time before and after cerebral ischemia/reperfusion （I/R）. Terminal deoxynucleotidyltransferasemediated dUTP biotin nick end labeling （TUNEI,） was perfornwd to dectect the apoptosis cells. The expressions of Bcl-2 and Bax in neuron of hippocampal CA I region were detected through immunohistochemistry method. Results： Positive cells were seen in all slices of cerebral isehemia/rcperfusion 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 CAI region increased obviously while the expression of Bax decreased 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 the expression of Bax. The effect of Batroxobin injection on cerebral 1/R was time dependent.
出处
《南京医科大学学报（自然科学版）》
CAS
CSCD
北大核心
2005年第10期697-699,F0002,共4页
Journal of Nanjing Medical University(Natural Sciences)
