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|

Ⅱ型糖尿病大鼠心梗后非梗死区心室重构的研究

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2010年第4期
页码:
520-523,636
栏目:
基础研究
出版日期:
2010-06-10

文章信息/Info

Title:
Ventricular remodeling in non-infarcted areas after myocardial infarction in type II diabetic rats
作者:
路军刘野郑强荪滕继伟李若愚张丽娜刘雄涛
第四军医大学唐都医院心内科,陕西 西安 710038
Author(s):
LU Jun LIU Ye ZHENG Qiang-sun TENG Ji-wei LI Ruo-yu ZHANG Li-na LIU Xiong-tao
Department of Cardiology, Tangdu Hospital, Fourth Military Medical University, Xi’an 710038, Shaanxi, China
关键词:
糖尿病心肌梗死心室重构大鼠
Keywords:
diabetes mellitus myocardial infarction ventricular remodeling rats
分类号:
R542.22
DOI:
-
文献标识码:
A
摘要:
目的: 对比观察糖尿病(DM)大鼠心肌梗死(MI)后非梗死区域心肌肥大、增殖分化和细胞凋亡的改变,探讨DM对MI后心室重构的影响。方法: 将实验大鼠分为正常对照组、糖尿病对照组、MI对照组及糖尿病MI组,从各组大鼠的左心室梗死周边取材,采用免疫组化染色法检测转化生长因子-β1(TGF-β1)、增殖细胞核抗原(PCNA),用末端脱氧核苷酸转移酶介导的dUTP末端缺口标记法(TUNEL)检测凋亡细胞,并进行对比分析。结果: DM大鼠MI后非梗死区域存在着明显的心肌肥大、增殖分化和细胞凋亡。试验表明,糖尿病MI组大鼠梗死区周边凋亡细胞及PCNA、TGF-β1的阳性率均明显高于DM对照组及MI对照组(P<0.01)。DM对照组大鼠梗死区周边凋亡细胞的比例明显高于MI对照组(P<0.01)。结论: DM可增强TGF-β1和PCNA的表达及增加细胞凋亡,三者可能为DM大鼠MI后高心律失常及高死亡率的病理生理基础。
Abstract:
AIM: To explore the effect of diabetes on ventricular remodeling in non-infarcted areas after myocardial infarction in type II diabetic rats by comparing changes of cardiac hypertrophy (TGF-β1), proliferation differentiation (PCNA) and apoptosis (TUNEL). METHODS: Sprague Dawley (SD) rats were randomly divided into blank group, diabetic group, infarcted group and infarcted diabetic group. Samples were obtained from the infarcted diabetic rats in non-infarcted area. Using immunohistochemistry and computer image processing technique, TGF-β1, PCNA and TUNEL expressions were examined in different groups (blank, diabetic, infarcted, infarcted diabetic). RESULTS: After myocardial infarction, the positive rates of TUNEL, PCNA, TGF-β1 in non-infarcted areas in infarcted diabetic group were significantly higher than those in the blank group, diabetic group and infarcted group (P<0.01). Compared with the infarcted group, the positive rate of TUNEL in non-infarcted areas in diabetic group was significantly higher. CONCLUSION: Diabetes increased expressions of cardiac hypertrophy, proliferation and apoptosis in non-infarcted regions, which may be the pathophysiological basis of high morbidity of ventricular arrhythmia and high mortality after myocardial infarction in diabetes.

参考文献/References

[1]Iliodromitis EK, Lazou A, Kremmastinos DT. Ischemic preconditioning: protection against myocardial necrosis and apoptosis[J]. Vasc Health Risk Manag, 2007, 3(5):629-637.

[2] Ikeda S, Hamada M. Relationship between cardiomyocyte cell death and cardiac function during hypertensive cardiac remodeling in Dalai rats[J]. Clin Sci, 2002, 102(3):329-335.

[3]Abbate A, Biondi-Zoccai GG, Bussani R, et al. Increased myocardial apoptosis in patients with unfavorable left ventricular remodeling and early symptomatic post-infarction heart failure[J]. J Am Coll Cardiol, 2003, 41(5):753-760.

[4]Koyama T, Xie Z, Suzuki J, et al. Expression of proliferating cell antigen in rat hearts subjected to transient ischemia followed by reperfusion[J]. Adv Exp Med Biol, 2003, 530:587-591.

[5]Palaniyandi SS, Nagai Y, Watanabe K. Chymase inhibition reduces the progression to heart failure after autoimmune myocarditis in rats[J]. Exp Biol Med, 2007, 232(9):1213-1221.

[6]李桂荣,李琳琳,毛新民. 改良高脂乳剂诱导2型糖尿病模型大鼠实验研究[J]. 新疆医科大学学报, 2007, 30(2):125-129.

[7]艾静,王宁,杜杰,等. Wistar大鼠2型糖尿病动物模型的建立[J]. 中国药理学通报, 2004, 20(11):1309-1312.

[8] Himori N, Matsuura A. A simple technique for occlusion and reperfusion of coronary artery in conscious rats[J]. Am J Physiol, 1989, 256(6 Pt 2):Hl7l9-H1725.

[9]Saraste A, Pulkki K, Kallajoki M, et al. Apoptosis in human acute myocardial infarction[J]. Circulation, 1997, 95(2):3202-3213.

[10]Palaniyandi SS, Nagai Y, Watanabe K. Chymase inhibition reduces the progression to heart failure after autoimmune myocarditis in rats[J]. Exp Biol Med, 2007, 232(9):1213-1221.

[11]Diniz GP, Carneiro-Ramos MS, Barreto-Chaves ML. Angiotensin type 1(AT1)and type 2(AT2)receptors mediate the increase in TGF-beta1 in thyroid hormone induced cardiac hypertrophy[J]. Pflugers Arch, 2007, 454(1):75-81.

[12]Woo YJ, Panlilio CM, Cheng RK. Myocardial regeneration therapy for ischemic cardiomyopathy with cyclin A2[J]. J Thorae Cardiovase Surg, 2007, 133(4):927-933.

[13]刘欣,康毅,贺慧杰,等. 糖尿病大鼠心肌TGF-β1表达及细胞凋亡的实验研究[J]. 中国病理生理杂志, 2007, 23(2):303-306.

[14]吕民,王越晖,张秀和,等. 心肌梗死大鼠TGF-β1 与I型胶原表达的研究[J]. 中国实验诊断学, 2005, 9(6):918-920.

[15]刘小青. TGF-β与心肌梗死后心脏修复[J]. 广西医学, 2009, 31(4):586-588.

[16]李家一,贾国良,程何祥,等. 心肌梗死模型中心肌细胞PCNA表达的特点及其意义[J]. 第四军医大学学报, 2004, 25(8):691-693.

[17]Jeremias I, Kupatt C, Martin-Villalba A, et al. Involvement of CD95/Apo1/Fas in cell death after myocardial ischemia[J]. Circulation, 2000, 102(8):915-20.

[18]Bojunga J, Nowak D, Mitrou PS, et al. oxidative treatment prevents activation of death-receptor- and mitochondrion-dependent apoptosis in the hearts of diabetic rats[J]. Diabetologia, 2004, 47(12):2072-2080.

[19]王国宏,袁申元,边延涛. 血管紧张素Ⅱ及其受体在大鼠糖尿病性心肌病发生中的作用[J]. 中华内分泌代谢杂志, 2001, 17(3):171.

备注/Memo

备注/Memo:
收稿日期:2009-07-27.通讯作者:郑强荪,主任医师,主要从事心律失常的临床和基础研究 Email:qingshu@fmmu.edu.cn 作者简介:路军,住院医师,硕士生Email:supermanlujun@vip.sina.com
更新日期/Last Update: 2010-05-20