首页> 外文期刊>Life sciences >Interleukin-18 reduces expression of cardiac tumor necrosis factor-alpha and atrial natriuretic peptide in a murine model of viral myocarditis.
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Interleukin-18 reduces expression of cardiac tumor necrosis factor-alpha and atrial natriuretic peptide in a murine model of viral myocarditis.

机译:白介素18降低病毒性心肌炎的小鼠模型中的心脏肿瘤坏死因子-α和心钠素的表达。

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摘要

Heart failure is generally believed to begin with myocyte damage caused by a variety of insults, including ischemia, toxin or myocardial infection. The proinflammatory cytokine, tumor necrosis factor-alpha (TNF-alpha), has been hypothesized to play a pathogenetic role in the transition from compensated to decompensated heart failure. Interleukin-18 (IL-18), a recently cloned cytokine synthesized by Kupffer cells, activates macrophages. We examined the therapeutic effect of IL-18 on the modulation of TNF-alpha gene expression in failing heart in a murine model of heart failure caused by viral myocarditis. The heart weight (HW)/ body weight (BW) ratio in IL-18 treated mice 7 days after viral inoculation was significantly lower (P<0.01) than in the untreated controls. Myocardial necrosis and inflammatory cell infiltration were significantly lower in IL-18 treated mice than untreated mice 5 and 7 days after inoculation. The expression of TNF-alpha mRNA in the myocardium was significantly lower on days 5 and 7 in IL-18 treated mice than in infected untreated mice. We conclude that concurrent systemic administration of IL-18 is beneficial in mice with myocarditis, and may be mediated through reduced expression of TNF-alpha in the heart.
机译:一般认为,心力衰竭始于多种损伤引起的心肌细胞损伤,包括缺血,毒素或心肌感染。促炎细胞因子肿瘤坏死因子-α(TNF-alpha)已被假定在从代偿性向失代偿性心力衰竭的过渡中起着致病作用。白细胞介素-18(IL-18)是由Kupffer细胞合成的最近克隆的细胞因子,可激活巨噬细胞。我们检查了IL-18对由病毒性心肌炎引起的心衰小鼠模型中衰竭心脏中TNF-α基因表达的调节作用。接种病毒7天后,经IL-18处理的小鼠的心重(HW)/体重(BW)比未处理的对照组显着降低(P <0.01)。接种后5天和7天,经IL-18处理的小鼠的心肌坏死和炎性细胞浸润明显低于未处理的小鼠。在IL-18处理的小鼠中,第5天和第7天,心肌中TNF-αmRNA的表达明显低于未感染的小鼠。我们得出的结论是,同时进行IL-18的全身给药对患有心肌炎的小鼠有益,并且可能通过降低TNF-α在心脏中的表达来介导。

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