不规则趋化因子在大鼠脑缺血再灌注损伤中的表达变化  

Expression changes in fractalkine induced by focal cerebral ischemia and reperfusion in rats

作　　者：周美君[1] 范学军[1] 燕丽娜[1] 周军[1] 

机构地区：[1]长沙市第四医院神经内科,410013

出　　处：《中华老年医学杂志》2015年第4期431-433,共3页Chinese Journal of Geriatrics

摘　　要：目的 观察不规则趋化因子Fractalkine（FKN）在大鼠缺血再灌注后脑皮质中的表达变化,探讨其规律及意义.方法 采用Longa线拴法制备大脑中动脉闭塞/再灌注（MCAO/R）模型,免疫组化法和蛋白免疫印迹法（Western blot）观察大鼠缺血区脑皮质中FKN的表达.结果 正常脑皮质中FKN少量表达（37.03±6.28）个,缺血再灌注3h组FKN表达升高（48.58±7.29）个（P＜0.05）,24 h组达高峰（112.08±8.26）个（P＜0.05）,然后下降,7d组FKN低水平表达（40.73±4.02）个（P＞0.05）.FKN在假手术组有一定水平的表达量0.527±0.002,再灌注后3h组开始上调至0.598±0.004（P＜0.05）,24 h组达高峰0.833±0.005（P＜0.05）,维持较高水平直至再灌注后48h为0.735±0.002（P＜0.05）,7d组回归基线水平0.533±0.004（P＞0.05）.结论 FKN在大鼠缺血再灌注后脑组织中表达上调,并动态变化,提示FKN可能参与了脑缺血再灌注损伤后炎症反应过程.Objective To investigate the expression changes of fractalkine （FKN）in focal cerebral ischemia and reperfusion penumbra,and to explore its variation law and role in the inflammation of cerebral ischemia-reperfusion injury.Methods The cerebral ischemia reperfusionmodel was established by intraluminal thread occlusion in the middle cerebral arteries occlusion （MCAO）.FKN protein expression in focal cerebral ischemia and reperfusion penumbra was detected by immunohistochemistry and Western blot.Results The results of immunohistochemistry stain showed that the chemokine FKN was expressed in a low level in the normal group and the sham operation group,and there were no significant differences among the two groups （P〉 0.05）.Compared with the humbers of FKN in normal group （37.03± 6.28） in focal cerebral ischemia and reperfusion penumbra,the expression of FKN in model group was increased after 3 h of reperfusion （48.58±7.29） （P〈0.05）,peaked at 24 h （112.08±8.26） （P〈0.05],and then decreased gradually at day 7 after reperfusion,but had no significant difference （40.73 ± 4.02） （P〉 0.05）.FKN was expressed in a low level in the sham operation group （0.527±0.002）,then up-regulated after 3 h of reperfusion [（0.598±0.004）,P〈0.05],peaked at 24 h [（0.833±0.005）,P〈0.05],maintained a high level till 48 h after reperfusion [（0.735±0.002）,P〈0.05],and return to baseline level at day 7 after reperfusion [（0.533±0.004）,P〉0.05].Conclusions Fractalkine is upregulated after focal cerebral ischemia/reperfusion,and has a dynamical change,which indicates that fractalkine might involve in the inflammatory process after cerebral ischemia-reperfusion injury.

关 键 词：缺血再灌注损伤 趋化因子 CX3C 大鼠 

分 类 号：R743.3[医药卫生—神经病学与精神病学]