CD59在小鼠脑缺血再灌注损伤中的表达及意义

Expression of CD59 in mice with cerebral ischemia-reperfusion injury and its significance

  • 摘要: 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2.166 7±0.408 3,再灌注后72 h评分降至0.833 3±0.408 3,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。

     

    Abstract: 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.

     

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