[1]向平,涂柳,陈沅.大鼠阿霉素所致心肌病过程中PI3K/AKT以及ERK1/2信号通路表达的改变[J].第三军医大学学报,2008,30(11):1071-1074.
 XIANG Ping,TU Liu,CHEN Yuan.PI3K/AKT and ERK1/2 signaling pathways in the process of cardiomyopathy induced by doxorubicin[J].J Third Mil Med Univ,2008,30(11):1071-1074.
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《第三军医大学学报》[ISSN:1000-5404/CN:51-1095/R]

卷:
30卷
期数:
2008年第11期
页码:
1071-1074
栏目:
论著
出版日期:
2008-06-15

文章信息/Info

Title:
PI3K/AKT and ERK1/2 signaling pathways in the process of cardiomyopathy induced by doxorubicin
作者:
向平涂柳陈沅
重庆医科大学:附属儿童医院心血管内科,生理学教研室
Author(s):
XIANG Ping TU Liu CHEN Yuan
Department of Cardiology, Children’s Hospital,Department of Physiology, Chongqing Medical University, Chongqing 400016, China
关键词:
阿霉素心肌病心脏毒性细胞凋亡信号通路
Keywords:
doxorubicin cardiomyopathy cardiotoxicity apoptosis signaling pathway
分类号:
R329.28; R542.2; R979.14
文献标志码:
A
摘要:
目的    研究阿霉素对心脏结构功能的影响以及此过程中部分相关信号通路的变化。    方法    用20只SD大鼠分为两组:阿霉素组(10只)和正常组(10只),观察阿霉素对心脏结构及功能改变,心肌细胞凋亡以及p-AKT与p-ERK1/2的蛋白水平。    结果    阿霉素注射11周后造成肌纤维排列紊乱,肌纤维丢失及肌浆空泡化,心脏功能尤其是收缩功能下降(FS与CO比较,P<0.01),心肌细胞凋亡增加,p-AKT与p-ERK1/2的蛋白水平较正常明显下降。    结论    阿霉素能明显造成心脏结构及功能的损伤,心肌细胞凋亡,PI3K/AKT与ERK1/2两条信号通路的变化可能参与到阿霉素的心脏毒性过程中。
Abstract:
Objective    To investigate the role of PI3K/AKT and ERK1/2 signaling pathways in the process of cardiomyopathy induced by doxorubicin (DOX).     Methods    Twenty SD rats were divided into two groups: DOX group (10 rats that were injected through caudal vein with 2.5 mg/kg DOX, once a week, for 6 weeks) and control group (10 rats). At 5th week after the end of DOX injection, the structural changes and functional damage were examined, and the apoptosis rate of cardiomyocytes and the expression levels of p-AKT and p-ERK1/2 were determined.     Results    Eleven weeks after the DOX injection, the myocardial pathological changes were mainly myofibrillar loss and cytoplasmic vacuolization. DOX could induce compensated heart function (the value of FS% was 34, P<0.01 as compared with control group). DOX caused cardiac cell apoptosis and the apoptosis ratio was 28.4% (P<0.01, as compared with control group). The expression of Bcl-2 increased to 126% (P>0.05) and Bax to 338% (P<0.05) of control level. In DOX group, phosphorylation of Akt was reduced to 12% (P<0.05) and that of ERK1/2 was reduced to 24% (P<0.05) of control level.     Conclusion    DOX can induce the damage of cardiac function and the apoptosis of cardiomyocytes, in which the PI3K/AKT and ERK1/2 signaling pathways may play important roles.

参考文献/References:

向平,涂柳,陈沅. 大鼠阿霉素所致心肌病过程中PI3K/AKT以及ERK1/2信号通路表达的改变[J].第三军医大学学报,2008,30(11):1071-1074.

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更新日期/Last Update: 2008-06-06