[1]张安,邓武,殷跃辉.甲亢性心肌病兔心肌血管紧张素转换酶和细胞外信号调节激酶的变化[J].第三军医大学学报,2007,29(22):2156-2159.
 ZHANG An,DENG Wu,YIN Yue-hui.Changes of ACE and ERK in rabbits with hyperthyroid cardiomyopathy induced by Levothyroxine[J].J Third Mil Med Univ,2007,29(22):2156-2159.
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甲亢性心肌病兔心肌血管紧张素转换酶和细胞外信号调节激酶的变化(/HTML )
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《第三军医大学学报》[ISSN:1000-5404/CN:51-1095/R]

卷:
29卷
期数:
2007年第22期
页码:
2156-2159
栏目:
论著
出版日期:
2007-11-30

文章信息/Info

Title:
Changes of ACE and ERK in rabbits with hyperthyroid cardiomyopathy induced by Levothyroxine
作者:
张安邓武 殷跃辉
重庆医科大学附属第二医院心血管内科
Author(s):
ZHANG An DENG Wu YIN Yue-hui
Department of Cardiovascular Disease, Second Affiliated Hospital of Chongqing Medical University, Chongqing  400010,China
关键词:
甲状腺功能亢进心肌病血管紧张素转换酶细胞外信号调节激酶
Keywords:
hyperthyroidism cardiomyopathy angiotensin converting enzyme extracellular signal-regulated kinase
分类号:
R345;R542.202;R581.1
文献标志码:
A
摘要:
目的  探讨甲亢性心肌病的发病机制。 方法  健康成年新西兰大白兔40只,按随机数字表法分为4组:空白对照组、左旋甲状腺素(L-Thy)组、咪哒普利组、缬沙坦组。L-Thy(45 μg· kg-1·d-1× 28 d)腹腔注射建立甲亢性心肌病模型,第28天收集心肌标本测定左右心室心肌肥厚指数, 光镜下观察心肌细胞结构,测定心肌细胞直径,Masson’s 染色测定胶原容积分数(collagen volume fraction, CVF),透射电镜观察心肌细胞超微结构改变, Western blot检测血管紧张素转换酶(angiotensin converting enzyme, ACE)、细胞外信号调节激酶(ERK)及磷酸化细胞外信号调节激酶(p-ERK)的蛋白表达。 结果  L-Thy可诱导心肌肥厚、心肌细胞结构改变以及纤维组织增生,ACE、ERK和p-ERK蛋白表达上调, ERK及p-ERK表达与心肌细胞平均直径和CVF呈正相关。咪哒普利和缬沙坦均可显著抑制L-Thy诱导的心肌细胞肥厚和纤维化,从而降低ERK、p-ERK的表达。 结论  肾素-血管紧张素系统(RAS)和ERK信号传导通路可能参与甲亢性心肌病的发病机制,ERK信号传导通路的激活可能与RAS有关, 咪哒普利和缬沙坦可以抑制ERK信号传导通路的激活并改善L-Thy诱导的心肌重构。
Abstract:
Objective    To explore  the  etiology  of  hyperthyroid cardiomyopathy.     Methods    Forty New Zealand rabbits were randomly and equally divided into 4 groups: control group, levothyroxine(L-Thy) group, imidapril group, and valsartan group. Except the control group, rabbit model of hyperthyroidism was established by daily intraperitoneal injections of L-Thy (45 μg·kg-1·d-1× 28 d), and the animals of later 2 groups received 0.5 mg/kg imidapril and 8 mg/kg valsartan respectively at same period. Ventricular tissues were collected at 4 weeks. Cardic hypertrophy index, cardiomyocyte diameter, structural and ultrastructural changes were detected. Cardiac fibrosis was displayed by Masson’s staining and collagen volume fraction (CVF) was measured using pathological image analytic system. Expressions of angiotensin converting enzyme (ACE), extracellular signal-regulated kinase (ERK), and phosphorylated ERK (p-ERK) were evaluated with Western blot analyses.  Results    Compared with control group, rabbits of L-Thy group displayed remarkable myocardial hypertrophy, extracellular matrix fibrosis, and morphological changes in both structure and ultrastructure. Western blot analysis revealed increased protein expressions of ACE,ERK and p-ERK proteins. ERK and p-ERK expressions were correlated positively well with both cardiomyocyte diameter and CVF. Both imidapril and valsartan alleviated cardiomyocyte hypertrophy, extracellular matrix fibrosis, and structural damage induced by L-Thy. Compared with L-Thy group, expressions of lower ERK and  p-ERK were found in both imidapril and valsartan groups.    Conclusion   Renin-angiotension system (RAS) and ERK signaling pathway may play important roles in hyperthyroid cardiomyopathy. Activated RAS is possibly responsible for activation of ERK signaling pathway. Imidapril and valsartan may inhibit activation of ERK signaling pathway and retarding myocardial remodeling in hyperthyroid cardiomyopathy induced by L-Thy.

参考文献/References:

张安,邓武, 殷跃辉.  甲亢性心肌病兔心肌血管紧张素转换酶和细胞外信号调节激酶的变化[J]. 第三军医大学学报, 2007, 29(22):2156-2159.

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更新日期/Last Update: 2008-07-01