晚期糖基化终产物受体在小鼠慢性阿霉素心脏毒性模型中的表达  

Expression of the receptor for advanced glycation end products in mice with chronic adriamycin-induced cardiotoxicity

作　　者：施盛锋 朱劲舟[2] 张瑞岩[2] 

机构地区：[1]江苏省海门市人民医院心血管内科,江苏海门226100 [2]上海交通大学医学院附属瑞金医院心血管内科,上海200025

出　　处：《解剖学报》2014年第4期550-554,共5页Acta Anatomica Sinica

基　　金：国家自然科学基金资助项目(81370401)

摘　　要：目的探讨晚期糖基化终产物受体(RAGE)在小鼠慢性阿霉素心脏毒性模型中的表达及其与化疗药相关心脏毒性的可能内在联系。方法通过多次腹腔注射阿霉素,建立小鼠慢性阿霉素心脏毒性模型,同时设立正常对照组(每组6只)。模型建立后采用超声心动图和组织病理学方法评价小鼠心脏功能及心肌损伤程度;通过免疫印迹及免疫组织化学检测小鼠心肌组织中RAGE表达变化。结果超声心动图检查显示,慢性阿霉素心脏毒性小鼠左室射血分数明显降低;病理学观察显示心肌组织中细胞损伤明显,同时伴有心室肥厚及心肌重构,提示小鼠慢性阿霉素心脏毒性模型建立成功。细胞和分子生物学观察发现,损伤心肌中RAGE表达显著升高。结论RAGE在慢性小鼠阿霉素心脏毒性模型中表达升高,提示其可能参与阿霉素相关心脏毒性的发生发展。Objective To study the expression of receptor for advanced glycation end products （ RAGE ） in chronic adriamycin （ ADR ）-induced cardiotoxicity mice . Method A mouse model of chronic cardiotoxicity was established by intraperitoneal injection of 5 mg/kg ADR once a week for continuous 3 weeks.Mice treated with the same volume of saline were used as control group （6 mice in each group）.Echocardiography and histopathological examination were used to evaluate the myocardial injury , cardiac function and ventricular remodeling .The expression of RAGE in cardiac tissues was detected by immunohistochemical staining and Western blotting .Results Echocardiography indicated that ADR-treated mice had reduced left ventricular ejection fraction , while histopathological analysis of cardiac tissues showed obvious cardiac damage . RAGE protein in cardiac tissues was highly expressed in chronic ADR-induced cardiotoxicity mice .Conclusion RAGE is highly induced and may be involved in the cardiotoxicity after ADR treatment .

关 键 词：阿霉素 晚期糖基化终产物受体 心肌 心脏超声 HE染色 免疫组织化学 免疫印迹法 小鼠 

分 类 号：R541.9[医药卫生—心血管疾病]