CAJ | 학술논문

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.
목적 관찰불규칙추화인자Fractalkine(FKN)재대서결혈재관주후뇌피질중적표체변화,탐토기규률급의의.방법 채용Longa선전법제비대뇌중동맥폐새/재관주(MCAO/R)모형,면역조화법화단백면역인적법(Western blot)관찰대서결혈구뇌피질중FKN적표체.결과 정상뇌피질중FKN소량표체(37.03±6.28)개,결혈재관주3h조FKN표체승고(48.58±7.29)개(P＜0.05),24 h조체고봉(112.08±8.26)개(P＜0.05),연후하강,7d조FKN저수평표체(40.73±4.02)개(P＞0.05).FKN재가수술조유일정수평적표체량0.527±0.002,재관주후3h조개시상조지0.598±0.004(P＜0.05),24 h조체고봉0.833±0.005(P＜0.05),유지교고수평직지재관주후48h위0.735±0.002(P＜0.05),7d조회귀기선수평0.533±0.004(P＞0.05).결론 FKN재대서결혈재관주후뇌조직중표체상조,병동태변화,제시FKN가능삼여료뇌결혈재관주손상후염증반응과정.
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.