CAJ | 학술논문

目的观察补体调节蛋白CD59在小鼠脑缺血-再灌注损伤过程中的表达变化情况及意义.方法采用线栓法制备小鼠大脑中动脉闭塞(middle cerebral artery occlusion,MCAO)模型,缺血1 h后再灌注.记录小鼠大脑神经功能缺失程度、脑组织病理的动态变化,应用免疫荧光组织化学法及荧光定量PCR法检测脑内补体调节蛋白CD59的表达变化.结果再灌注后24 h神经功能缺失评分最高为2.1667±0.4083,再灌注后72 h评分降至0.8333±0.4083,再灌注后96 h评分为0,恢复正常.脑组织病理损伤再灌注后24 h后最严重,脑内补体调节蛋白CD59至再灌注后24 h达最低,再灌注96 h基本恢复正常.补体调节蛋白CD59表达水平与脑组织病理损伤和神经功能缺损评分呈负相关.结论脑缺血-再灌注后补体调节蛋白CD59的表达水平发生显著变化,其可能参与脑缺血-再灌注后的免疫损伤过程.
목적관찰보체조절단백CD59재소서뇌결혈-재관주손상과정중적표체변화정황급의의.방법채용선전법제비소서대뇌중동맥폐새(middle cerebral artery occlusion,MCAO)모형,결혈1 h후재관주.기록소서대뇌신경공능결실정도、뇌조직병리적동태변화,응용면역형광조직화학법급형광정량PCR법검측뇌내보체조절단백CD59적표체변화.결과재관주후24 h신경공능결실평분최고위2.1667±0.4083,재관주후72 h평분강지0.8333±0.4083,재관주후96 h평분위0,회복정상.뇌조직병리손상재관주후24 h후최엄중,뇌내보체조절단백CD59지재관주후24 h체최저,재관주96 h기본회복정상.보체조절단백CD59표체수평여뇌조직병리손상화신경공능결손평분정부상관.결론뇌결혈-재관주후보체조절단백CD59적표체수평발생현저변화,기가능삼여뇌결혈-재관주후적면역손상과정.
Objective To observe the expression of complement regulatory protein CD59 in mice with cerebral ischemia-reperfusion (I/R) injury and its significance. Methods A mouse middle cerebral artery occlusion (MACO) model was established with filament method. One hour after ischemia, the mice were subjected to reperfusion. Their cranial neurological deficit and brain tissue pathological lesion were recorded. Expression of complement regulatory protein CD59 was detected by immunohistochemistry and RT-PCR, respectively. Results The neurological deficit score was 2.166 7±0.408 3, 0.833 3±0.408 3 and 0, respectively, at 24, 72 and 96 h after reperfusion. The brain tissue pathological lesion was the severest at 24 h after reperfusion. The expression level of complement regulatory protein CD59 was the lowest at 24 h and almost retuned to normal at 96 h after reperfusion. The expression level of complement regulatory protein CD59 was negatively related with brain pathological injury and neurological deficit score. Conclusion The expression level of complement regulatory protein CD59 changes significantly after cerebral I/R, indicating that CD59 may be involved in cerebral I/R injury.