我们的网站为什么显示成这样?

可能因为您的浏览器不支持样式,您可以更新您的浏览器到最新版本,以获取对此功能的支持,访问下面的网站,获取关于浏览器的信息:

|本期目录/Table of Contents|

福辛普利对大鼠缺血/再灌注损伤心肌细胞Caspase3表达的影响(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2006年第6期
页码:
614-616
栏目:
基础研究
出版日期:
2006-12-25

文章信息/Info

Title:
Effect of Fosinopril on regulation of Caspase3 in ischemia and reperfusion injury rat myocardium
作者:
张志国秦玲赵学忠
吉林大学第一医院心内科,吉林 长春130021
Author(s):
ZHANG Zhi-guo QIN Ling ZHAO Xue-zhong
Department of Cardiology, First Hospital of Jilin University, Changchun Jilin 130021, China
关键词:
心肌缺血再灌注损伤福辛普利Caspase-3
Keywords:
myocardial ischemiareperfusion injuryFosinprilCaspase-3
分类号:
R542.2
DOI:
-
文献标识码:
A
摘要:
目的 观察福辛普利对大鼠心肌缺血/再灌注损伤后细胞凋亡关键酶Caspase-3表达的影响。方法 结扎大鼠左冠状动脉前降支,30 min后松开结扎线,假手术组只穿线不结扎,大鼠随机分为假手术组、缺血/再灌注组、福辛普利组(20 mg/kg)。福辛普利组分别于术前24 h及术前2 h灌胃给药,观察24 h后心肌细胞电镜下的形态改变和Caspase3 mRNA的表达。结果 福辛普利组电镜下肌丝肌节清晰,而缺血再灌注组闰盘结构不清,肌丝断裂,大鼠心肌Caspase-3 mRNA表达灰度值福辛普利组为0.37±0.03,缺血/再灌注组为1.14±0.05(P<0.01)。结论 福辛普利可以使心肌缺血/再灌注后的Caspase-3的表达下降。
Abstract:
AIM To study the protective effect of Fosinopril on ischemia and reperfusion rat myocardium and the Caspase3 expression in myocardium. METHODS Wistar rats were randomly divided into three groups: Control group (n=8), IschemiaReperfusion group (n=8), in which the left anterior descending of coronary artery was occluded for 30 min followed by 24 hours reperfusion and Fosinopril (20 mg/kg) group (n=8). Medication was fed through gastric gavage 24 hour and 2 hour before occlusion and the Caspase3 expression in myocardium was observed. RESULTS The expression of Caspase3 mRNA in Fosinpril group was less than that of IschemiaReperfusion group (0.37±0.03 vs 1.14±0.05 and 0.39±0.03 vs 1.14±0.05,P<0.01) respectively. CONCLUSION Fosinpril can reduce Caspase3 expression in myocardium, thus protecting ischemia and reperfusion rat myocardium.

参考文献/References

[1] 罗义,李卓仁,郭南山 心血管疾病中的细胞凋亡 [J]. 中华内科杂志,1998,37(3):207-209.

[2] Williams JG, Kubelik AR, Livak KJ, et al. DNA polymorphisms amplified by arbitrary primers are useful as genetic markers [J]. Nucleic Acids Res,1990,18(22):6531-6535.

[3] Fliss H, Gattinger D. Apoptosis in ischemic and reperfused rat myocardium [J]. Circ Res,1996,79(5):949-956.

[4] Goldenberg I, Grossman E, Jacobson KA, et al. Angiotensin Ⅱinduced apoptosis in rat cardiomyocyte culture: a possible role of AT1 and AT2 receptors [J]. J Hypertens, 2001,19(9):1681-1689.

[5] Wallach D, Varfolomeev EE, Malinin NL, et al. Tumor necrosis factor receptor and Fas signaling mechanisms [J]. Annu Rev Immunol,1999,17:331-367.

[6] Liu JJ, Peng L, Bradley CJ, et al. Increased apoptosis in the heart of genetic hypertension, associated with increased fibroblasts [J]. Cardiovasc Res, 2000 ,45(3):729-735.

[7] Steindel M, Dias Neto E, Pinto CJ, et al. Randomly amplified polymorphic DNA (RAPD) and isoenzyme analysis of Trypanosoma rangeli strains [J]. J Eukaryot Microbiol,1994,41 (3): 261-267.

备注/Memo

备注/Memo:
收稿日期:2005-10-21.基金项目:吉林省科技发展计划资助项目(No.990581-3) 通讯作者:赵学忠,教授,主要从事冠心病发病机制及诊治研究 Tel:(0431)5612416 Email:zhxzh@medmail.com 作者简介:张志国,医师,硕士 Tel:(0431)5612217 Email:zg529@163.com
更新日期/Last Update: