N-acetylcysteine suppresses the progression of ventricular remodeling in acute myocarditis: studies in an experimental autoimmune myocarditis (EAM) model.
N-acetylcysteine suppresses the progression of ventricular remodeling in acute myocarditis: studies in an experimental autoimmune myocarditis (EAM) model.
复制标题
N-乙酰半胱氨酸抑制急性心肌炎心室重构的进展：实验性自身免疫性心肌炎（EAM）模型的研究。
DOI：
10.1253/circj.cj-10-0673
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发表时间：
2011
期刊：
影响因子：
--
通讯作者：
T. Izumi
中科院分区：
文献类型：
--
作者：
S. Niwano;H. Niwano;Sae Sasaki;H. Fukaya;Masaru Yuge;R. Imaki;Yoji Machida;T. Izumi
背景
本文研究了实验性自身免疫性心肌炎（EAM）大鼠心肌电重构和结构重构，其特征为动作电位时程（APD）延长、Kv4.2下调和细胞浸润。由于活性氧（ROS）被推测在促进这种重塑中起作用，因此评价了N-乙酰半胱氨酸（NAC）对心室重塑进展的影响。
方法和结果
用猪心肌肌球蛋白免疫6周龄刘易斯大鼠。在免疫后第10-11天，将NAC（0、1、10、100 mg）腹腔注射到EAM和对照组大鼠。实验第14天，采用实时荧光定量逆转录聚合酶链反应（RT-PCR）检测心肌细胞Kv4.2 mRNA的表达水平，观察心肌细胞的电生理变化，结果表明，EAM大鼠表现为典型的急性心肌炎，APD延长，Kv4.2表达减少。NAC能明显抑制心肌炎和心电图改变，并呈剂量依赖性（P<0.05）。NAC 100 mg组大鼠的心肌炎几乎完全消失，但死亡率增加。NAC 1 mg对大鼠心肌炎的抑制作用不明显，但对APD延长和Kv4.2降低有明显的抑制作用（P<0.05）。
结论
NAC治疗抑制EAM大鼠的心室重构。这可能表明氧化应激在心肌炎急性期引起重塑和心肌炎本身中的作用。
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.
影响因子：
20.1
作者：
Kaab, S;Nuss, HB;Tomaselli, GF
通讯作者：
Tomaselli, GF