延迟肢体缺血后处理对大鼠急性脑梗死后脑水肿的影响及其机制探讨  

The effect and mechanism of delayed limb ischemic postconditioning on brain edema after acute cerebral ischemia in rats

作　　者：陈历[1] 季一飞[1] 龙继发[1] 杜鑫[1] 张翼[1] 熊健[1] 王运锋[1] 

机构地区：[1]川北医学院第二临床学院.南充市中心医院神经内科,四川南充637000

出　　处：《西部医学》2016年第12期1638-1642,共5页Medical Journal of West China

基　　金：国家自然科学基金(81271317);四川省科技厅课题(2012JY0043)

摘　　要：目的观察延迟肢体缺血后处理对大鼠脑梗死后脑水肿的干预作用及Eph受体酪氨酸激酶-A2（EphA2）的变化规律，探讨延迟肢体缺血后处理减轻大鼠脑梗死后脑水肿的机制。方法采用线栓法建立大鼠大脑中动脉闭塞模型。采用轮流夹闭双下肢股动脉主干，2min缺血／2min再灌注，各5个周期，连续5d进行肢体缺血后处理。比较脑组织含水量、伊文思兰（EB）含量，以及运用免疫组织化学染色检测各组EphA2的表达。结果从2～5d，单纯再灌注各时间组脑组织含水量均明显高于延迟肢体缺血后处理各时间组（P〈0．05）；单纯再灌注各时间组脑组织EB含量均明显高于延迟肢体缺血后处理各时间组（P〈0．05）；与单纯再灌注纽各时间点比较，延迟肢体缺血后处理组EphA2的阳性细胞数均明显降低（P〈0．05）。单纯再灌注组于1d时EphA2就开始增多，2d达高峰，3d时出现下降；延迟肢体缺血后处理变化趋势相同，但高峰值明显低于前者。结论延迟肢体缺血后处理可能减轻脑梗死后脑水肿程度，其机制可能与抑制EphA2的表达有关。Objectives We explored the effect of delayed limb ischemic postconditioning on cerebral edema, analyzed the change law of EphA2 after acute cerebral ischemia in rats and explored the mechanism on brain edema in delayed limb iscbemic postconditioning. Methods We used MCAO model with clipping the double femoral artery by turns 2 rain ischemia/2 rain reperfusion, 5 cycles and 5 consecutive days. The water content in brain tissue, EB content and the expression of EphA2 in each group were detected by immunohistochemical staining. Results From the second day to the fifth day, the water content in the simple ischemia reperfusion group was significantly higher than that in delayed limb ischemic posteonditioning group （P;0.05） at each time point. The EB content in the simple Isehemia reperfusion group was significantly higher than that of delayed limb isehemie posteonditioning group （P〈0.05）. The number of EphA2 positive cells in delayed limb iscbemic postconditioning group were significantly lower than that at each time point in simple ischemia reperfusion group （P〈0.05）. The number of EphA2 positive cells in simple isehemia reperfusion group increased from the first day, which reached the peak at the second day, and begun to fall at the third day. There was the same change tendency in delayed limb isehemic postconditioning, but the peak value was significantly lower than that of the simple lschemia reperfusion group. Conclusions Delayed Limb Ischemie postconditioning may reduce the degree of brain edema after cerebral infarction, and its mechanism may be related to inhibition of EphA2 expression.

关 键 词：缺血再灌注损伤 EPHA2 延迟肢体缺血后处理 

分 类 号：R543.31[医药卫生—心血管疾病]