›› 2010, Vol. 41 ›› Issue (2): 232-236.doi: 10.3969/j.issn.0529-1356.2010.02.013

• 论著 • 上一篇    下一篇

氯沙坦对大鼠慢性心力衰竭的干预作用

欧叶涛*; 田国忠 ;王建杰 ;张东东; 陈乃峰 ;王培军; 扈清云 ;韩曦   

  1. 佳木斯大学基础医学院解剖学教研室,黑龙江 佳木斯 154007
  • 收稿日期:2009-04-09 修回日期:2009-06-08 出版日期:2010-04-06
  • 通讯作者: 欧叶涛

Losartan intervenes chronic heart failure of rats

  1. Department of Anatomy, Basic Medical School, Jiamusi Uuniversity, Heilongjiang Jiamusi 154007,China
  • Received:2009-04-09 Revised:2009-06-08 Online:2010-04-06
  • Contact: OU Ye-tao

关键词: 氯沙坦, 慢性心衰, 细胞外信号调节激酶, 氨基末端激酶, 促分裂原活化蛋白激酶, 免疫组织化学, 反转录-聚合酶连反应, 大鼠

Abstract: Objective To study the reasons and mechanism of cardiomyocyte apoptosis in chronic heart failure by using Losartan and to provide a theoretical basis for the treatment of chronic heart failure. Methods The models of chronic heart failure were produced by injecting Adriamycin and Losartan as intervention agents, the expression of apoptotic protein Bax, Bcl-2 and channel protein ERK1, JNK1 and P38MAPK were detected by immunohistochemistry and RT-PCR.Cardiomyocyte apoptosis and myocardial ultrastructure are detected by transmission electron microscopy and TUNEL staining. Results Compared with the model group of heart failure, after Losartan treatment, the ultra structure of myocardial cells were significantly improved, Apoptosis index was decreased significantly (EM>P /EM><0.01), The level of Bax and JNK1 decreased (Bax χSUP>2/SUP> =6.6149, EM>P/EM> =0.0078; JNK1 EM>q/EM> =22.156,EM>P /EM><0.01). However, the expressions of ERK1 and Bcl-2 were significantly increased (ERK1 EM>q /EM>=15.3514,EM>P /EM><0.01;Bcl-2 χSUP>2/SUP> =6.81,EM>P

Key words: Losartan, Chronic heart failure, Extracellular signal-regulated kinase, Jun N-terminal kinase, Mitogen-activated protein kinase, Immunohistochemistry, RT-PCR, Rat

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