吸氧预处理对大鼠脑缺血再灌注损伤AIF核转移的抑制作用

Effect of oxygen-breathing preconditioning on translocation of apoptosis-inducing factor( AIF) in focal cerebral ischemia/reperfusion injury in rats

目的探讨吸氧预处理对大鼠脑缺血再灌注损伤凋亡诱导因子(AIF)核转移的影响,揭示吸氧预处理治疗的分子机制。方法将78只SD大鼠随机分为3组:缺血再灌注组、吸氧预处理组、假手术组。缺血再灌注组用线栓法制作大鼠大脑右侧中动脉阻塞模型,2 h后实现再灌注。吸氧预处理组术前24 h持续吸入100%纯氧24 h。假手术组除不插入线栓外其它步骤同模型组。按再灌注时间再分为12 h、24 h、48 h组,用免疫组织化学和免疫印迹(Western-blot)法,检测缺血侧海马CA1区AIF核移位情况。结果免疫组化染色和Western blot检测可见吸氧预处理组和缺血再灌注组在不同时间点AIF蛋白发生核移位,AIF阳性细胞数及AIF蛋白含量较缺血再灌注组减少,差异有统计学意义(P<0.05)。结论吸氧预处理对脑缺血再灌注损伤神经细胞保护作用,其机制之一可能是对AIF核移位的抑制。

Objective To investigate the effect of oxygen-breathing preconditioning on translocation of apoptosis-inducing factor（AIF） and neuronal apoptosis in focal cerebral ischemia/reperfusion injury in rats. Methods 78 male SD rats were used as research subjects and randomly divided into three groups：ischemia/reperfusion vehicle group, oxygen-breathing preconditioning pretreatment group and sham-operated group. Embolization thread was inserted into all rats except those in the sham-operated group for 2 hours to establish middle cerebral artery occlusion models,24 h continuous inhaled 100% pure oxygen to oxygen-breathing preconditioning pretreatment group for 24 b. Other steps of the sham-operated group were the same as the model group except not inserting line plug. In the reperfusion time divided into 12 h,24 h,48 h group, using immunohistochemistry and Western blot （Western blot） method to detect nuclear translocation of AIF in bippocampal CA1 area of isebemia. Results AIF protein nuclear translocation was detected in oxygen pretreatment group and ischemla-reper- fusion group at different time points by immunohistochemical staining and western blot method,compared with ischemiareperfusion group ,the number of AIF positive cells and AIF protein content decreased in oxygen pretreatment group with statistically significant （ P 〈 0.05 ）. Conclusion Oxygen preconditioning has a protective effect on neuronal apoptosis of cerebral ischemia-reperfusion injury,one of the mechanism is probably the inhibition of AIF nuclear translocation.