小鼠近交系病毒性心肌炎中硫氧还蛋白表达的差异。

M. Miyamoto, C. Kishimoto, K. Shioji, H. Nakamura, S. Toyokuni, Y. Nakayama, M. Kita, J. Yodoi, S. Sasayama
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引用次数: 15

摘要

氧化还原调节机制可能参与病毒性心肌炎的发病机制,硫氧还蛋白(TRX)是一种含有氧化还原活性序列的小多功能蛋白。本研究研究了急性柯萨奇病毒B3型心肌炎小鼠近交系(DBA/2小鼠重度心肌炎、BALB/c小鼠中度心肌炎和C57BL/6小鼠轻度心肌炎)中TRX的组织病理学和表达特点。硫氧还蛋白上调,其表达与疾病的严重程度相关。此外,8-羟基-2'-脱氧鸟苷是氧化应激的既定标志物,在受损的肌细胞中同时呈阳性。因此,小鼠病毒性心肌炎的急性炎症刺激可能特异性诱导TRX,急性病毒性心肌炎的严重程度和发展可能受细胞氧化还原状态的调控。
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Difference in thioredoxin expression in viral myocarditis in inbred strains of mice.
Redox regulating mechanisms may be involved in the pathogenesis of viral myocarditis and thioredoxin (TRX) is a small multifunctional protein that contains a redox active sequence. The present study investigated the histopathology and characteristics of TRX expression in acute coxsackievirus B3 myocarditis in inbred strains of mice (severe myocarditis in DBA/2 mice, moderate myocarditis in BALB/c mice and mild myocarditis in C57BL/6 mice). Thioredoxin was upregulated and its expression correlated with the severity of the disease. In addition, 8-hydroxy-2'-deoxyguanosine, which is an established marker for oxidative stress, was concominantly positive in damaged myocytes. Thus, TRX may be specifically induced by the acute inflammatory stimuli in murine viral myocarditis, and the severity and development of acute viral myocarditis may be regulated by the cellular redox state.
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