| 心力衰竭兔左室Ito、Ik1通道蛋白表达变化及比索洛尔干预作用 |
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| 引用本文： | 陈文婷,李溪,倪雅娟,卢群,卓小桢,王亭忠,沈建,岳鑫,马爱群. 心力衰竭兔左室Ito、Ik1通道蛋白表达变化及比索洛尔干预作用[J]. 中国分子心脏病学杂志, 2013, 13(1): 419-423 |
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| 作者姓名： | 陈文婷 李溪 倪雅娟 卢群 卓小桢 王亭忠 沈建 岳鑫 马爱群 |
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| 作者单位： | 1. 西安交通大学医学院第一附属医院心血管内科;环境与疾病相关基因教育部重点实验室(心血管离子通道病研究室);陕西省分子心脏病学重点实验室,雁塔西路277号,陕西西安710061
2. 西安交通大学医学院第一附属医院心血管内科;环境与疾病相关基因教育部重点实验室(心血管离子通道病研究室);陕西省分子心脏病学重点实验室,雁塔西路277号,陕西西安710061;宁夏医科大学总医院心脑血管病医院,黄河东路宁安东巷,宁夏银川750004 |
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| 基金项目： | 国家自然科学基金重点项目(30830051) |
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| 摘 要： | 目的观察心力衰竭兔左室心肌细胞Ito、Ik1通道蛋白表达变化及比索洛尔的干预作用,探讨心力衰竭时室性心律失常的发生机制及比索洛尔可能的抗心律失常机制。方法 39只新西兰兔随机分为假手术组(SO)、心力衰竭组(HF)及比索洛尔干预组(BF),以容量负荷联合压力超负荷方法构建心力衰竭兔模型,评价模型成功后,予比索洛尔干预6周;用Westernblot法测定瞬时外向钾电流(Ito)、内向整流钾电流(Ik1)通道蛋白的表达水平。结果①HF组兔心动超声示左房、左室增大,心脏收缩功能和舒张功能减低,BNP水平明显升高,心体比明显增大;比索洛尔干预6周可部分逆转上述变化;②与SO组相比,心力衰竭时左室心肌细胞Kv4.3(介导Ito,f)、Kv1.4(介导Ito,s)及Kir2.1(介导Ik1)蛋白表达水平降低;比索洛尔干预6周后Kv4.3、Kv1.4、Kir2.1蛋白表达较心力衰竭组均有所增加。结论心力衰竭兔左室心肌细胞Kv4.3、Kv1.4、Kir2.1蛋白表达明显下降,可能是心力衰竭时室性心律失常发生的分子基础。比索洛尔干预后可部分逆转Kv4.3、Kv1.4、Kir2.1蛋白表达的下调,可能是其抗心律失常的分子机制。
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| 关 键 词： | 心力衰竭 钾离子通道 蛋白表达 β受体阻滞剂 |
Bisoprolol reverse down-regulated Ito and IK1 in left ventricle of rabbits with heart failure |
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| Chen Wen-Ting,Li Xi, Ni Ya-Juan, Lu Qun, Zhuo Xiao-Zhen, Wang Ting-Zhong, Shen Jian, Yue Xin, Ma Ai-Qun. Bisoprolol reverse down-regulated Ito and IK1 in left ventricle of rabbits with heart failure[J]. Molecular Cardiology of China, 2013, 13(1): 419-423 |
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| Authors: | Chen Wen-Ting Li Xi Ni Ya-Juan Lu Qun Zhuo Xiao-Zhen Wang Ting-Zhong Shen Jian Yue Xin Ma Ai-Qun |
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| Affiliation: | *. Department of Cardiovascular Medicine, First Affiliated Hospital of Medical College of Xi’an Jiaotong University; Institute of Cardiovascular Channelopathy, Key Laboratory of Environment and Genes Related to Diseases (Xi’an Jiaotong University), Ministry of Education; Key Laboratory of Molecular Cardiology, Shannxi Province; No.277 Yanta West Road, Xi’an, Shaanxi 710061, P.R. China |
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| Abstract: | Objective To investigate the effects of β -blocker, bisoprolol, on the protein expression of transient outward potassium current （Ito） and inward rectifier potassium current （Ik1） in left ventricle of rabbits with heart failure. Methods Thirty New Zealand rabbits were randomized into 3 groups： sham operation group （SO）, heart failure group （HF） and heart failure with bisoprolol intervention group（BF）. HF rabbits were induced by volume overload combined with pressure overload procedures. Electrocardiographic variables and plasma brain natriuretie peptide （BNP） level were tested to evaluate the cardiac function. The protein expression oflto （mediated by Kv4.3 and Kv1.4） and Ik1 （mediated by Kir2.1） in left ventricle were tested by Western blot analysis. Results Compared with SO, HF rabbits exhibited left ventricular and atrial enlargement, systolic and diastolic dysfimetion, along with increased plasma BNP level and heart weight ratio. After treatment with bisoprolol for 6 weeks, those indexes were all partly reversed. Western blot results showed that protein expression of Kv4.3, Kv1.4 and Kir2.1 were significantly decreased, and 6 weeks bisoprolol intervention can restore these down regulation expression of Kv4.3, Kv1.4 and Kir2.1. ConcLusion The decreased expression of Kv4.3, Kv1.4 and Kir2.1 might underline the molecular mechanism of ventricular arrhythmia in heart failure. Bisoprolol may have anti-arrhythmia effect by reversing the down- regulation of Kv4.3, Kir1.4 and Kir2.1 protein expression in left ventricle. |
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| Keywords: | Heart failure Potassium channels Protein expression β-blocker |
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