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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 investigate the expression of advanced glycation end-products receptor (RAGE) in mouse chronic adriamycin cardiotoxicity model and its possible relationship with the chemotherapeutic drug-related cardiotoxicity. Methods The chronic adriamycin cardiotoxicity model was established by intraperitoneal injection of doxorubicin. At the same time, normal control group (6 mice in each group) was established. The model was established by echocardiography and histopathological evaluation of cardiac function and myocardial injury in mice; by Western blot and immunohistochemical detection of myocardial tissue RAGE expression changes. Results Echocardiography showed that the left ventricular ejection fraction of chronic doxorubicin-induced cardiotoxicity mice was significantly lower than that of the control group. Pathological examination revealed obvious cell injury in myocardium with concomitant ventricular hypertrophy and myocardial remodeling. Cardiotoxicity model was established successfully. Cell and molecular biology found that RAGE expression was significantly increased in injured myocardium. Conclusions RAGE is up-regulated in adriamycin-induced cardiotoxicity in chronic mice, suggesting that RAGE might be involved in the development of adriamycin-related cardiotoxicity.