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首页> 外文期刊>Journal of Medical Colleges of PLA >Effects and mechanism of different adrenergic receptor antagonists on left ventricular hypertrophy subsequent to coarctation of abdominal aorta in rats
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Effects and mechanism of different adrenergic receptor antagonists on left ventricular hypertrophy subsequent to coarctation of abdominal aorta in rats

机译:不同肾上腺素能受体拮抗剂对大鼠腹主动脉缩窄后左室肥厚的影响及其机制

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Objective: To study the changes of a collagen-binding protein (Colligin) and myosin heavy chain isofrom (α/β-MHC) gene and protein in left ventricular hypertrophy subsequent to coarctation of abdominal aorta in rats and the effects of three kinds of adrenergic receptor blockers: Carvedilol (CAR), Metoprolol (MET) and Terazosin (TER) on these changes, and to elucidate the effects and new mechanism of CAR on left ventricular hypertrophy regression. Methods: A model of hypertrophy induced by coarctation of abdominal aorta(CAA) was used in this study. Thirty two male wislar rats were divided randomly into four groups 4 weeks after CAA operation: CAA, CAR, MET and TER. Hemodynamics, ventricular remodeling parameters, expressions of Colligin and α/β-MHC mRNA, protein expressions of Collagen Ⅰ/Ⅲ and Colligin were investigated in the four groups and sham operation group. Results: Left ventricle hypertrophy was observed clearly 16 weeks after operation. The ratio of α/β-MHC mRNA decreased, while expressions of CollagenⅠ /Ⅲ proteins and Colligin mRNA/protein increased( P < 0.05) . CAR could ameliorate left ventricle hypertrophy prior to MET and TER. CAR could also change the expressions of α/β-MHC, CollagenⅠ / Ⅲ and Colligin in both gene and protein levels ( P < 0. 05). while MET and TER have no effect on them ( P > 0.05) . Conclusion: The effects of CAR on extracellular matrix proteins and MHC isoform shift regression of left ventricle may be due to antiproliferative or antioxidative mechanism, which was independent of beta-adrenergic receptor antagonist.
机译:目的:研究大鼠腹主动脉缩窄后左心室肥大中胶原结合蛋白(Colligin)和肌球蛋白重链异构体(α/β-MHC)基因和蛋白的变化以及三种肾上腺素的影响。受体阻滞剂:卡维地洛(CAR),美托洛尔(MET)和特拉唑嗪(TER)对这些变化的影响,并阐明了CAR对左心室肥大消退的作用和新机制。方法:采用腹主动脉缩窄引起的肥大模型。 CAA术后4周,将32只雄性维斯拉大鼠随机分为4组:CAA,CAR,MET和TER。分别于四组和假手术组观察血流动力学,心室重构参数,Colligin,α/β-MHCmRNA的表达,Ⅰ/Ⅲ型胶原蛋白和Colligin的蛋白表达。结果:术后16周清晰观察到左心室肥大。 α/β-MHCmRNA的比例降低,而胶原Ⅰ/Ⅲ蛋白和Colligin mRNA /蛋白的表达升高(P <0.05)。在MET和TER之前,CAR可以改善左心室肥大。 CAR还可以在基因和蛋白质水平上改变α/β-MHC,Ⅰ/Ⅲ型胶原和Colligin的表达(P <0。05)。而MET和TER对它们没有影响(P> 0.05)。结论:CAR对左心室细胞外基质蛋白和MHC亚型转移的影响可能是由于抗增殖或抗氧化机制,与β-肾上腺素能受体拮抗剂无关。

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