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目的探讨重组人促红细胞生成素(r-HuEPO)对大鼠局灶性脑缺血再灌注炎症损伤的保护机制。方法采用线栓法制备大鼠局灶性大脑中动脉栓塞(MCAO)模型,应用ELISA方法检测r-HuEPO治疗前后缺血侧脑皮质TNF-α含量变化,应用Western blot检测缺血侧脑皮质p38 MAPK表达的变化。结果与假手术组相比,缺血再灌注组脑皮质TNF-α、磷酸化p38 MAPK表达水平明显增加,r-HuEPO可抑制缺血再灌注脑皮质TNF-α增加及磷酸化p38 MAPK表达。结论 r-HuEPO可能通过抑制磷酸化p38 MAPK表达,减少炎症因子TNF-α的释放而抑制脑缺血再灌注损伤炎症反应。
Objective To investigate the protective mechanism of recombinant human erythropoietin (r-HuEPO) on inflammatory injury induced by focal cerebral ischemia-reperfusion in rats. Methods The focal middle cerebral artery occlusion (MCAO) model was established by thread occlusion. The content of TNF-α in ischemic cortex was detected by ELISA before and after treatment with r-HuEPO. Western blot was used to detect the expression of p38 Changes in MAPK expression. Results Compared with the sham operation group, the expression of TNF-α and phospho-p38 MAPK in cerebral cortex increased significantly after ischemia-reperfusion, and r-HuEPO could inhibit the increase of TNF-α and the phosphorylation of p38 MAPK in cerebral cortex after ischemia-reperfusion. Conclusion r-HuEPO may inhibit the inflammatory response of cerebral ischemia-reperfusion injury by inhibiting the expression of phosphorylated p38 MAPK and decreasing the release of inflammatory cytokines TNF-α.