Attenuation of oxidative stress and cardiac dysfunction by bisoprolol in an animal model of dilated cardiomyopathy
Attenuation of oxidative stress and cardiac dysfunction by bisoprolol in an animal model of dilated cardiomyopathy
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DOI：
10.1016/j.bbrc.2006.09.026
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发表时间：
2006-11-10
影响因子：
3.1
通讯作者：
Iwase, Mitsunori
中科院分区：
文献类型：
--
作者：
Ichihara, Sahoko;Yamada, Yoshiji;Iwase, Mitsunori
氧化应激是扩张型心肌病的重要易感因素。我们研究了比索洛尔（一种β 1选择性肾上腺素受体阻滞剂）对扩张型心肌病模型中氧化应激和心功能不全发生的影响。用比索洛尔（5 mg/kg/天）或溶剂处理8周龄雄性TO-2和对照仓鼠4周。比索洛尔治疗可预防TO-2仓鼠心功能不全的进展。该药物不影响NADPH氧化酶活性的增加，但阻止了TO-2仓鼠左心室中线粒体锰依赖性超氧化物歧化酶活性和表达的降低以及白细胞介素-1 β和肿瘤坏死因子-α浓度的增加。因此，比索洛尔减缓心功能不全的发展可能部分是由于左心室中氧化应激和促炎细胞因子水平相关增加的正常化。(c)2006年爱思唯尔公司All rights reserved.
Oxidative stress is an important susceptibility factor for dilated cardiomyopathy. We have investigated the effects of bisoprolol, a beta(1)-selective adrenoceptor blocker, on oxidative stress and the development of cardiac dysfunction in a model of dilated cardiomyopathy. Male TO-2 and control hamsters at 8 weeks of age were treated with bisoprolol (5 mg/kg per day) or vehicle for 4 weeks. Treatment with bisoprolol prevented the progression of cardiac dysfunction in TO-2 hamsters. This drug did not affect the increase in NADPH oxidase activity but prevented the reduction in activity and expression of mitochondrial manganese-dependent superoxide dismutase as well as the increases in the concentrations of interleukin-1 beta and tumor necrosis factor-alpha in the left ventricle of TO-2 hamsters. Attenuation of the development of cardiac dysfunction by bisoprolol may thus result in part from normalization of the associated increases in the levels of oxidative stress and pro-inflammatory cytokines in the left ventricle. (c) 2006 Elsevier Inc. All rights reserved.