促红细胞生成素对脑缺血再灌注炎症损伤的抑制作用

The Inhibitory Effect of EPO on Injury from Inflammation of Cerebral Ischemia-reperfusion

目的观察促红细胞生成素在局灶性脑缺血再灌注模型大鼠中对NF-κB、COX-2表达的影响,探讨促红细胞生成素在本过程中对炎症反应是否发挥抑制作用。方法健康SD大鼠70只。大鼠经过相应处理后,得到的组织标本分别通过免疫组化和Western Blot方法,分析大鼠海马组织中NF-κB和COX-2的表达差异。结果各处理组与缺血再灌注组相比,大鼠的神经功能学评分明显下降(P<0.01),NF-κB及COX-2表达均明显减少(P<0.01),PDTC组COX-2的表达仍较正常组偏高(P<0.01);EPO组和PDTC+EPO组大鼠神经功能学评分较PDTC组明显下降(P<0.01),而EPO组和PDTC+EPO组内COX-2蛋白表达量较PDTC组COX-2蛋白表达明显减少(P<0.01);大鼠神经功能缺损评分及COX-2的表达在EPO组和PDTC+EPO组之间差异无统计学意义(P>0.05)。结论实验表明促红细胞生成素降低大鼠海马区COX-2蛋白表达减轻脑缺血再灌注炎症反应的作用是通过两条途径实现的。

Objective To investigate the influence of EPO on the expression of NF- κB and COX- 2 in model rats with focal cerebral ischemia- reperfusion,and to explore whether EPO has any inhibitory effect on the inflammation. Methods 70 healthy SD rats were selected and divided into 5 groups： control,ischemia- reperfusion,EPO,PTDC and PDTC ＋ EPO group. All the brain tissue specimens obtained after the handling of the rats were used to analyze the difference in the expression of NF- κB and COX- 2 in the hippocampus of the rats with the method of immunohistochemistry and Western Blot. Results In comparison with those of the ischemia- reperfusion group,the neurological score of the rats in other groups significantly decreased（ P〈0. 01） and the expression of both NF- κB and COX- 2 declined remarkably（ P〈0. 01）,the expression of the latter one in the PDTC group still higher than that of the control group（ P〈0. 01）. The neurological score and the expression of COX- 2 of the rats in the EPO and the PDTC ＋ EPO groups both declined obviously compared with those of the PDTC group（ P〈0. 01）. There was no statistically significant difference in the neurological score and COX- 2 expression between the EPO and the PDTC ＋ EPO groups（ P〉0. 05）. Conclusions The experiment suggests that it is by 2 ways that EPO reduces the expression of COX- 2 in the hippocampus of the rats with focal cerebral ischemi- reperfusion injury in order to exert the inhibitory effect on the inflammation of the injury.