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首页> 外文期刊>Life sciences >Ginsenoside Re prevents angiotensin II-induced gap-junction remodeling by activation of PPARγ in isolated beating rat atria
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Ginsenoside Re prevents angiotensin II-induced gap-junction remodeling by activation of PPARγ in isolated beating rat atria

机译：人参皂甙再次通过孤立的殴打大鼠Atria激活PPARγ的激活来预防血管紧张素II诱导的间隙改造

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Abstract Aims Ginsenoside Re (G-Re), a major ginsenoside in ginseng, has many beneficial pharmacological effects on negative cardiac contractility, electromechanical alternans, antiarrhythmia, angiogenic regeneration and cardiac electrophysiological function. However, effects of G-Re on gap-junction remodeling are unclear. Therefore, this study aimed to investigate the effect of G-Re on angiotensin II (Ang II)-induced downregulation of connexin-40 (CX40) and -43 (CX43) in beating rat left atria. Main methods In this study, the isolated perfused beating rat atrial model was used and atrial gap-junction remodeling was induced by Ang II. In vivo hemodynamic experiments were analyzed with a biological recorder. Changes in protein expression were analyzed by western blot. Key findings G-Re attenuated Ang II-induced abnormal changes in heart rate, MAP, LVESP, LVEDP, +dp/dt max, ?dp/dt min, P wave amplitude, P-R interval and P wave length. This indicated a dose-dependent preventive role against Ang II-induced hyper hemodynamics in rats. Atrial activities of p38 mitogen-activated protein kinase (MAPK), nuclear factor kappa-B (NF-κB) and activator protein 1 (AP-1) were significantly increased by Ang II, as was expression of atrial collagen I and matrix metalloproteinase 2 (MMP2). Atrial CX40 and CX43 expression was downregulated by Ang II. These Ang II-induced atrial effects were blocked by G-Re, as well as rosiglitazone, an agonist of peroxisome proliferator-activated receptor γ (PPARγ), in a dose-dependent manner. However, this inhibition was abolished by the PPARγ inhibitor GW9662. Significance G-Re may suppress Ang II-induced downregulation of CX40 and CX43, by activating PPARγ signaling, in isolated perfused beating rat atria.
机译：摘要目标人参皂苷Re（G-Re）是人参中的主要人参皂苷，对负心性收缩力，机电障碍，抗心律失常，血管生成再生和心脏电生理学功能具有许多有益的药理作用。然而，G-RE对间隙结重新耦合的影响尚不清楚。因此，该研究旨在探讨G-RE对血管紧张素II（Ang II）的影响 - 诱导Connexin-40（CX40）和-43（CX43）的下调在击败Atria。主要方法在本研究中，使用分离的灌注搏动大鼠心房模型，Ang II诱导心房间隙结重新兴。用生物记录仪分析体内血液动力学实验。通过Western印迹分析蛋白质表达的变化。主要发现G-Re衰减Ang II诱导的心率，地图，LVESP，LVEDP，+ DP / DT MAX，ΔDP/ DT min，P波幅度，P-R间隔和P波长的异常变化。这表明了对大鼠Ang II诱导的高血动力学的剂量依赖性预防作用。 Ang II显着增加了P38丝裂原激活的蛋白激酶（MAPK），核因子Kappa-B（NF-κB）和活化剂蛋白1（AP-1）的心房活动，如心房胶原蛋白I和基质金属蛋白酶2的表达，显着增加（mmp2）。通过Ang II下调心房CX40和CX43表达。这些Ang II诱导的心房效应被G-Re，以及罗基列酮（Rosiglitazone），以剂量依赖性方式封闭过氧化物体增殖物激活受体γ（PPARγ）的激动剂。然而，PPARγ抑制剂GW9662废除了这种抑制。通过激活PPARγ信号传导，在分离的灌注搏动大鼠Atria中，显着性G-Re可以抑制CX40和CX43的下调CX40和CX43的下调。

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