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β肾上腺素受体过度激动致大鼠心肌细胞凋亡及Fas、Bcl2蛋白表达的实验研究(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2005年第3期
页码:
232-234
栏目:
基础研究
出版日期:
2005-05-05

文章信息/Info

Title:
The study on the expression of Fas and Bcl2 with myocyte apoptosis during the cardiac injury induced by βadrenergic overactivation
作者:
屈百鸣1;  俞坚武1; 赵仲生2; 茹国庆2; 徐文娟2
浙江省人民医院：1. 心内科，2. 病理科，浙江 杭州 310014
Author(s):
QU Baiming1;  YU Jianwu1;  ZHAO Zhongsheng2;  RU Guoqing2;  XU Wenjuan2
1.Department of Cardiology, 2.Department of pathology, Zhejiang Provincial Hospital, Hangzhou, Zhejiang 310014, China
关键词:
β肾上腺素受体; 异丙肾上腺素; 心肌细胞; 凋亡; Fas; Bcl2; 大鼠
Keywords:
βadrenergic;  isoproterenol ; myocardium;  apoptosis;  Fas;  Bcl2;  rats
分类号:
R541.1
DOI:
-
文献标识码:
A
摘要:
目的 探讨β肾上腺素受体（βAR）过度激动致大鼠心肌损伤时，心肌细胞凋亡相关蛋白Fas、Bcl2表达改变及心肌细胞凋亡的意义。方法 动物模型仿用异丙肾上腺素皮下注射方法。心肌组织切片分别行免疫组化染色及HE、TUNEL检测。结果 βAR过度激动致大鼠心肌损伤时，Fas、Bcl2蛋白皆上调表达（P<0.01），Fas蛋白表达上调更为显著（P<0.01），心肌损伤6 h、72 h段凋亡指数分别为7.6±1.5、14.8±4.1。结论 βAR过度激动致大鼠心肌损伤时，心肌细胞凋亡是参与损伤的重要病理机制之一，可能是导致心力衰竭的一个关键因素， Fas、Bcl2蛋白的表达在其调控过程中表现出显著的差异。
Abstract:
AIM To investigate the expression of Fas and Bcl2 and the significance of myocyte apoptosis during the cardiac injury induced by βadrenergic overactivated in rats. METHODS The rats were treated with subcutaneous injection of isoproterenol (ISO). Fas and Bcl2 protein was identified by immunohistochemical technique. Apoptotic myocytes were stained in situ by TUNEL, Myocardial damage stained with hematoxylin and eosin was examined. RESULTS The expression of Fas and Bcl2 was both upregulated (P<0.01 and P<0.01), and the degree in Fas expression was more higher (P<0.01). At 6 and 72 hour with cardiac injury, the apoptosis index was 7.6±1.5、14.8±4.1 respectively. CONCLUSION Our study suggests that the cardiomyocyte apoptosis is one of the important pathogenesis involved in cardiac insufficiency during the myocardium damage induced by the βadrenergic overactivated, and there is significantly difference between the expression of Fas and Bcl2 with the high level in the regulation of cardiomyocytes apoptosis.

参考文献/References

［1］ 李为民，孔一慧，田颖，等. β3受体激动剂对心力衰竭大鼠β1、β2、β3肾上腺素能受体mRNA表达水平的实验研究［J］. 中华心血管病杂志，2003，31（1）:11-16.

［2］ Lee P, Sata M, Lefer DJ, et al. Fas pathway is a critical mediator of cardiac myocyte death and MI during ischemiareperfusion in vivo［J］. Am J Physiol Heart Circ Physiol, 2003, 284(2):H456-H463.

［3］ Zhao ZQ, Budde JM, Morris C, et al. Adenosine attenuates reperfusioninduced apoptotic cell death by modulating expression of Bcl2 and Bax proteins［J］. J Mol Cell Cardiol, 2001, 33(1):57-68.

［4］ 刘兴德，陈运贞. 蛋白激酶C活化对大鼠缺血/再灌注心肌细胞凋亡和Bcl2表达的影响［J］. 中国病理生理杂志，2002，18（8）: 949-953.

［5］ Yaniv G, Shilkrut M, Lotan R, et al. Hypoxia predisposes neonatal rat ventricular myocytes to apoptosis induced by activation of the Fas (CD95/Apo1) receptor: Fas activation and apoptosis in hypoxic myocytes［J］. Cardiovasc Res, 2002, 54(3):611-623.

［6］ 郭海涛，朱妙章，张荣怀，等. 血管钠肽抑制对心肌细胞收缩的增强作用［J］. 心脏杂志，2004，16（3）: 204-206

［7］ Saito S, Hiroi Y, Zou Y, et al. betaAdrenergic pathway induces apoptosis through calcineurin activation in cardiac myocytes［J］. J Biol Chem, 2000, 275 (44) : 34528-34533.

备注/Memo

备注/Memo:
收稿日期：2004-09-28.
更新日期/Last Update: 2010-01-05