单核细胞趋化蛋白-1在大鼠脑缺血再灌注损伤中的表达变化

Changes in Expression of MCP-1 Induced by Focal Cerebral Ischemia and Reperfusion in Rats

目的观察大鼠大脑中动脉闭塞(MCAO)后再灌注不同时间点单核细胞趋化蛋白-1(MCP-1)与基因表达的变化,以探讨其在脑缺血再灌注损伤中的意义。方法建立大鼠局灶性脑缺血再灌注模型,用免疫荧光双标染色、逆转录-聚合酶链反应(RT-PCR)技术检测MCP-1蛋白表达、mRNA转录水平。结果(1)缺血再灌注后缺血脑组织中存在表达MCP-1/NSE和MCP-1/GFAP双阳性细胞,提示神经元和神经胶质细胞是产生MCP-1的细胞来源之一。(2)各缺血再灌注组MCP-1 mRNA表达均高于假手术组,再灌注1 h MCP-1的mRNA转录即有升高,且随时间延长而进一步升高,24 h达到高峰之后逐渐下降。结论脑缺血再灌注引起MCP-1表达上调,提示MCP-1可能参与了局灶性脑缺血再灌注损伤。

Objective To investigate the expression of Monocyte Chemoattractant Protein-1 （MCP-1） in focal cerebral ischemia in rats, and to explore its role in ischemic neuronal injury. Methods The model of middle cerebral artery occlusion （MCAO） followed by reperfusion in rats was established. The immunoreactivity and mRNA level of MCP-1 were evaluated by double-labeled immuno-fluorescent staining and reverse transcriptionpolymerase chain reaction （RT-PCR） technique. Results （1） The double-labeled immunostaining for MCP-1 and neuron specific enolase （NSE） or glial fibrillary acidic protein （GFAP） showed that MCP-1 positive neurons and MCP-1 positive astrocytes were observed in the focal ischemic brain. （2） Compared with the SS group, the transcription of MCP-1 mRNA was elevated at 1 h and peaked at 24 h after reperfusion, then decreased gradually. Conclusions It is suggested that up-regulation of MCP-1 might be a key event in the neuronal injury induced by focal cerebral ischemia reperfusion.