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Impact of Selenium on NFκB Translocation in Isoproterenol-Induced Myocardial Infarction in Rats

机译:硒对异丙肾上腺素诱发的大鼠心肌梗死NFκB易位的影响

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摘要

NFκB is a major transcription factor that controls the expression of various genes. Its activation is a complex process that can be triggered by many agents and one among them is reactive oxygen species. The aim of this study was to investigate the effect of selenium on NFκB activation in rats induced with myocardial infarction by isoproterenol (ISP). The markers of myocardial infarction showed increased activity in the serum of rats induced with ISP compared to the group that was pretreated with selenium along with ISP. Cellular selenium status was also found to be very low in the ISP-induced group of rats. The concentration of cytosolic NFκB was comparatively lower in the ISP group than in the group treated with selenium and ISP. Whereas higher levels of NFκB were found in the nuclear extract of the ISP-treated animals than in the selenium + ISP group. Elevated levels of malondialdehyde, hydroperoxides, and conjugated diens in the ISP-treated rats revealed the higher levels of oxidative stress in this group. Thus, our studies reveal the inhibitory effect of selenium in the nuclear translocation of NFκB during myocardial infarction. Histopathological studies of the heart also support the cardioprotective role of selenium.
机译:NFκB是控制各种基因表达的主要转录因子。它的活化是一个复杂的过程,可由许多物质触发,其中之一是活性氧。这项研究的目的是研究硒对异丙肾上腺素(ISP)诱发的心肌梗死大鼠的NFκB活化的影响。与用硒和ISP预处理的组相比,心肌梗塞的标志物在ISP诱导的大鼠血清中具有增强的活性。在ISP诱导的大鼠组中,细胞硒状态也很低。 ISP组的胞浆NFκB浓度比硒和ISP处理组低。而在ISP处理过的动物的核提取物中发现的NFκB水平高于硒+ ISP组。 ISP处理的大鼠中丙二醛,氢过氧化物和共轭二烯的水平升高,表明该组的氧化应激水平较高。因此,我们的研究揭示了硒对心肌梗死期间NFκB核移位的抑制作用。心脏的组织病理学研究也支持硒的心脏保护作用。

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