促红细胞生成素对压力超负荷小鼠心肌保护作用的相关分子机制  

The protective effect and possible related mechanism of erythropoietin on the pressure overload-induced left ventricular dysfunction in mice

作　　者：王琬婷 冯照强 白静慧 WANG Wan-ting1, FENGZhao-qiang2, BAI Jing-hui1(1.Department of General Medicine, and 2. Department of Hepatobiliary Surgery, Cancer Hospital of China Medical University, Liaoning Cancer Hospital, Shenyang 110042, Chin)

机构地区：[1]中国医科大学肿瘤医院辽宁省肿瘤医院综合内科,辽宁沈阳110042 [2]中国医科大学肿瘤医院辽宁省肿瘤医院肝胆胰外科,辽宁沈阳110042

出　　处：《解剖科学进展》2018年第2期122-125,共4页Progress of Anatomical Sciences

基　　金：辽宁省科技攻关项目(2013225021);辽宁省博士启动基金(20141185)

摘　　要：目的探讨促红细胞生成素(EPO)对压力超负荷小鼠心肌保护作用的分子机制。方法采用主动脉弓缩窄术(TAC)的方法建立小鼠模型,小鼠随机分为假手术组(Sham)、模型组(TAC-PBS)和EPO2000U/Kg治疗组(TAC-EPO2000)。术后8周,测定各组小鼠心肌毛细血管密度及生存率,Western blot方法检测各组小鼠心肌组织p Akt/Akt、p-STAT3/STAT3、p-e NOS/e NOS、p-p38/p38、p-ERK/ERK-1、p-JNK/JNK的表达。结果 EPO治疗能显著提高TAC小鼠生存率(P<0.05)。与TAC-PBS组比较,TAC-EPO2000心肌组织p-STAT3、p Akt和p-e NOS的表达水平显著增多(P<0.05),p-p38的表达水平显著减少(P<0.05),p-ERK/ERK-1,p-JNK/JNK则无明显差异(P>0.05)。各组小鼠心肌毛细血管密度没有明显差异。结论 EPO对压力超负荷小鼠心肌保护作用可能与调控p-STAT3、p Akt、p-e NOS和p-p38的表达相关。Objective To study the protective effect and possible related mechanism of erythropoietin on the pressure overload-induced left ventricular dysfunction in mice. Methods Mice model was established by aortic arch constriction（TAC）, the mice were randomly divided into sham group, model group（TAC-PBS） and EPO 2000U/Kg treatment group （TAC-EPO2000）. The myocardial capillary density and survival rate were measured 8 weeks after operation. The expression of pAkt/Akt, p-STAT3/STAT3, p-eNOS/eNOS, p-p38/p38, p-ERK/ERK-1 and p-JNK/JNK in myocardium was detected by Western blot. Results EPO treatment could significantly increase the survival rate of TAC mice（P〈0.05）. Compared with TAC-PBS group, the expression levels of p-STAT3, p-Akt and p-eNOS in the myocardium were increased significantly in TAC-EPO2000 （P〈0.05）, but decreased for p-p38 expression（P〈0.05）, with no significant difference between p-ERK/ERK-1 and p-JNK/JNK （P〉0.05） expression and in myocardial capillary density in all groups （P〉0.05）. Conclusion The protective effect of EPO on myocardium in stress overload mice might be realized by regulating the expression of p-STAT3, pAkt, p-eNOS and p-p38.

关 键 词：促红细胞生成素 心肌保护 左心室功能障碍 小鼠 

分 类 号：R541[医药卫生—心血管疾病]