摘要
目的研究全脑缺血再灌注损伤后JUN蛋白在大鼠海马的表达及热休克预处理对其表达的影响。方法以四血管法建立全脑缺血再灌注模型。将大鼠置于42℃中15 min行热休克预处理,全脑缺血6 min后行2 h、6 h、12 h、24 h3、d、5 d再灌注后处死,取海马脑组织行HE染色、JUN蛋白免疫组化染色,TUNEL法检测凋亡细胞。结果缺血再灌注后2 h JUN蛋白在CA1区开始表达,6 h达到高峰,5 d时仍有表达;CA3区JUN蛋白的表达弱于CA1区(P<0.05);同时CA1区细胞损伤明显。热休克预处理组JUN蛋白表达在CA1和CA3区相应时点减弱(P<0.05),细胞损伤轻微,凋亡细胞减少(P<0.05)。结论全脑缺血再灌注损伤后JUN蛋白过度表达参与了神经元损伤过程,热休克预处理通过下调JUN蛋白过度表达具有脑保护作用。
Objective To investigate the expression of c-jun in hippocampus of rats after global cerebral ischemia/reperfusion and the effect of heat shock precondition on it. Methods Global cerebral ischemia/ reperfusion model was produced by 4-VO method. Rats were put at 42 ℃ for 15 min as heat shock precondition. After 6 min ischemia and 2 h, 6 h, 12 h, 24 h, 3 d and 5 d reperfusion, the rats were executed and brains were removed. HE, immunohistochemical and TUNEL staining of brain tissue sections were performed. Results In CA1 of the IR group, JUN expressed at 2 h after global cerebral ischemia/reperfusion, peaked at 6h and continued until 5 d. JUN expression in CA3 was weaker than that in CA1. The cellular damage in CA1 was more obvious than that in CA3. Expression of JUN in CA1 and CA3 of HP group was weaker than that in IR group at corresponding time （P〈0.05）. At the same time, cellular damage were weaker than that in IR group and the number of apoptosis cells decreased （P 〈 0. 05）. Conclusion Overexpression of JUN after global cerebral ischemia/reperfusion participates in the neural injury procedure and heat shock precondition performes its brain protective function through its suppressive effect on the overexpression of c-jun.
出处
《西安交通大学学报（医学版）》
CAS
CSCD
北大核心
2006年第4期337-340,共4页
Journal of Xi’an Jiaotong University（Medical Sciences）
基金
陕西省科技攻关项目[No.2005K13-G4(1)]
