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首页> 外文期刊>Circulation journal >N-acetylcysteine suppresses the progression of ventricular remodeling in acute myocarditis: studies in an experimental autoimmune myocarditis (EAM) model.
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N-acetylcysteine suppresses the progression of ventricular remodeling in acute myocarditis: studies in an experimental autoimmune myocarditis (EAM) model.

机译:N-乙酰半胱氨酸抑制急性心肌炎的心室重构的进展:在实验性自身免疫性心肌炎(EAM)模型中的研究。

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BACKGROUND: Electrical and structural remodeling, characterized by prolonged action potential duration (APD), Kv4.2 downregulation and cellular infiltration were studied in rat experimental autoimmune myocarditis (EAM). Because the reactive oxygen species (ROS) has been speculated to play a role in the promotion of such remodeling, the effect of N-acetylcysteine (NAC) on the progression of ventricular remodeling was evaluated. METHODS AND RESULTS: Six-week-old Lewis rats were immunized with porcine cardiac myosin. On Days 10-11 after the immunization, NAC (0, 1, 10, or 100mg) was injected intraperitoneally to EAM and control rats. On Day 14, the electrophysiological parameters were evaluated and the expression levels of the mRNA were examined by quantitative real-time reverse-transcription polymerase chain reaction (RT-PCR).The EAM rats exhibited a typical acute myocarditis with prolonged APD and reduced Kv4.2 expression as previously reported. The myocarditis and electrical changes were significantly suppressed by NAC-treatment in a dose-dependent manner (P<0.05). In rats with 100mg NAC, the myocarditis was almost totally negated although the mortality increased. In rats with 1mg NAC, the suppression of myocarditis was not obvious, but APD prolongation and Kv4.2 reduction was attenuated (P<0.05). CONCLUSIONS: The NAC treatment suppressed ventricular remodeling in the EAM rats. This may indicate the role of oxidative stress in causing remodeling and myocarditis itself in the acute phase of myocarditis.
机译:背景:在大鼠实验性自身免疫性心肌炎(EAM)中,研究了以动作电位持续时间(APD),Kv4.2下调和细胞浸润为特征的电和结构重塑。由于已经推测活性氧(ROS)在促进此类重塑中发挥作用,因此评估了N-乙酰半胱氨酸(NAC)对心室重塑进展的影响。方法和结果:六周龄的Lewis大鼠用猪心肌肌球蛋白免疫。免疫后第10-11天,将NAC(0、1、10或100mg)腹膜内注射至EAM和对照组大鼠。在第14天,通过实时定量逆转录聚合酶链反应(RT-PCR)评估电生理参数并检测mRNA的表达水平。EAM大鼠表现出典型的急性心肌炎,其APD延长且Kv4降低。 2表达如先前报道。 NAC治疗以剂量依赖性方式显着抑制心肌炎和电变化(P <0.05)。在具有100mg NAC的大鼠中,尽管死亡率增加,但心肌炎几乎完全被否定。 NAC 1mg的大鼠对心肌炎的抑制作用不明显,但APD延长和Kv4.2降低减弱(P <0.05)。结论:NAC治疗抑制了EAM大鼠的心室重构。这可能表明氧化应激在心肌炎的急性期中引起重构和心肌炎本身的作用。

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