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目的研究促红细胞生成素对幼兔心肌缺血再灌注损伤的保护作用与PI3K-AKT信号转导途径的关系。方法 30只日本大耳白幼兔随机分为对照组与EPO预处理组,每组15只。提前24 h,EPO预处理组经腹腔注射EPO(5 000 U/kg),对照组经腹腔注射同体积生理盐水。建立Langendroff幼兔离体心脏灌注模型,应用免疫组化法观察缺血再复灌120 min心肌组织PI3K、AKT及caspase 9表达情况,TUNNEL法检测细胞凋亡。结果 EPO组缺血再灌注后的心肌PI3K及AKT表达较对照组明显增多;caspase 9表达较对照组明显减少,两组差异存在统计学意义(P<0.01);EPO组凋亡细胞较对照组明显较少,两组差异存在统计学意义(P<0.01)。结论促红细胞生成素通过PI3K-AKT信号转导途径的抗凋亡作用而减轻幼兔心肌缺血再灌注损伤。
Objective To investigate the protective effect of erythropoietin on myocardial ischemia-reperfusion injury in rabbits and its relationship with PI3K-AKT signal transduction pathway. Methods Thirty Japanese white rabbits were randomly divided into control group and EPO pretreatment group, 15 rats in each group. At 24 h, the EPO pretreatment group was injected with EPO (5000U / kg) intraperitoneally, and the control group was injected intraperitoneally with the same volume of normal saline. The isolated Langendorff rabbit model of cardiac perfusion was established. The expression of PI3K, AKT and caspase 9 in myocardial tissue was detected by immunohistochemistry at 120 min after ischemia / reperfusion, and the apoptosis was detected by TUNNEL. Results Compared with control group, the expression of PI3K and AKT in EPO group was significantly increased after ischemia / reperfusion; the expression of caspase 9 was significantly decreased in the EPO group compared with the control group (P <0.01); the apoptosis of EPO group was higher than that in the control group Significantly less, there was a significant difference between the two groups (P <0.01). Conclusion Erythropoietin attenuates myocardial ischemia-reperfusion injury in immature rabbits through the anti-apoptotic effect of PI3K-AKT signal transduction pathway.