摘要
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 study the effect of erythropoietin（EPO） on PI3-K/Akt signal pathway of myocardial ischemia-reperfusion injury（I/R） in immature rabbits. Methods Thirty immature rabbits were randomly divided into two groups （n = 15/greup ）, The rabbits were intraperi- toneally injected with 2 ml of normal saline in control group, or 5 000 U/kg of EPO in treated group 24 h before I/R. The Langendorff isolat- ed perfused heart model was established, and the myocardial expression of PI3K, AKT and Caspase 9 were examined by immunohistochem- istry in 2 h after repeffusion. To monitor the myocardial apoptosis,we performed TUNEL in 2 h after reperfusion. Results The expression of myocardial PI3K and AKT in EPO group was significantly higher in EPO-treated group than those in control group. In EPO-treated group, the expression of myocardial caspase 9 was significantly lower than that in control group. The average optical density of myocardial PI3K, AKT and caspase 9 were significantly different between both groups （P 〈 0.01 ）.The number of apoptotic cell was significantly fewer in EPO- treated group than that in control group. The myocardial apoptosis index （AI）was significantly different between two groups （P 〈 0.01 ）. Conclusion EPO pretreatment can influence the PI3-K/Akt signal pathway and decrease the myocardial apoptosis,and significantly reduce the myocardial ischemia-reperfusion（I/R） injury in immature rabbits.
出处
《中国医科大学学报》
CAS
CSCD
北大核心
2010年第9期710-712,716,共4页
Journal of China Medical University
基金
辽宁省自然科学基金资助项目(20092107)
