阿霉素性心力衰竭模型的氧化应激和凋亡机制  

Mechanisms of heart failure induced by adriamycin

作　　者：吴伟康[1] 杨辉[2] 赵明奇[1] 

机构地区：[1]中山大学中山医学院病理生理学教研室,广东广州510089 [2]广州医学院第一附属医院中医科,广东广州510120

出　　处：《中国病理生理杂志》2004年第8期1437-1439,共3页Chinese Journal of Pathophysiology

基　　金：广东省中医药局课题 (No .995 5 9) ;广东省自然科学基金课题 (No.0 0 132 3)

摘　　要：目的 :观察阿霉素 (ADR)复制慢性心力衰竭模型的心功能、氧化应激和心肌细胞凋亡发生情况。方法 :TBA法测定丙二醛 (MDA)含量、邻苯三酚法测定超氧化物歧化酶 (SOD)活性动态变化 ,TUNEL法检测细胞凋亡 ,免疫组化检测P5 3蛋白含量 ,RT -PCR法检测p5 3mRNA表达。结果 :ADR引起大鼠心功能显著降低的同时MDA含量显著增加 ,SOD活性显著下降 ,心肌细胞发生凋亡 ,心肌组织p5 3mRNA表达增加 ,P5 3蛋白合成明显增多。结论 :阿霉素性心力衰竭模型有显著的氧化应激反应和细胞凋亡发生 ,p5 3基因在其凋亡发生机制中有一定作用。AIM: To investigate the changes of cardiac function, oxidative stress and apoptosis in myocardium of rat model of heart failure induced by adriamycin (ADR). METHODS: At the end of the study, we observed content of malondialdehyde (MDA), activity of superoxide dismutase (SOD) and apoptosis. Expression of P53 protein and p53 mRNA were measured with immunohistochemical method and RT-PCR, respectively. RESULTS: Our data showed that content of MDA increased, activity of SOD decreased and apoptosis in myocardium happened while cardiac function decreased after ADR treatment. p53 gene expression and P53 protein obviously increased in heart failure group. CONCLUSION: There were oxidative stress and apoptosis occurred significantly in a model of heart failure induced by ADR. p53 gene might play an important role in the apoptosis. Correlation analyses suggested that apoptosis in myocardium is related to oxidative stress in ADR-induced heart failure.

关 键 词：多柔比星 心力衰竭 应激 细胞凋亡 基因 P53 蛋白质P53 

分 类 号：R363[医药卫生—病理学]