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Differential expression of myocardial heat shock proteins in rats acutely exposed to fluoride

机译:急性氟中毒大鼠心肌热休克蛋白的差异表达

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Acute fluoride (F?) toxicity is known to cause severe cardiac complications and leads to sudden heart failure. Previously, we reported that increased myocardial oxidative damage, apoptosis, altered cytoskeleton and AMPK signaling proteins associated with energy deprivation in acute F? induced cardiac dysfunction. The present study was aimed to decipher the status of myocardial heat shock proteins (Hsps-Hsp27, Hsp32, Hsp40, Hsp60, Hsp70, Hsp90) and heat shock transcription factor 1 (Hsf1) in acute F?-intoxicated rats. In order to study the expression of myocardial Hsps, male Wistar rats were treated with single oral doses of 45 and 90?mg/kg F? for 24?h. The expression levels of myocardial Hsps were determined using RT-PCR, western blotting, and immunohistochemical studies. Acute F?-intoxicated rats showed elevated levels of both the transcripts and protein expression of Hsf1, Hsp27, Hsp32, Hsp60, and Hsp70 when compared to control. In addition, the expression levels of Hsp40 and Hsp90 were significantly declined in a dose-dependent fashion in F?-treated animals. Our result suggests that differential expression of Hsps in the rat myocardium could serve as a balance between pro-survival and death signal during acute F?-induced heart failure.
机译:众所周知,急性氟中毒会导致严重的心脏并发症,并导致突发性心力衰竭。以前,我们报道了急性F2中与能量剥夺有关的心肌氧化损伤,细胞凋亡,细胞骨架和AMPK信号蛋白改变增加。诱发心脏功能障碍。本研究的目的是破译急性F2中毒大鼠心肌热休克蛋白(Hsps-Hsp27,Hsp32,Hsp40,Hsp60,Hsp70,Hsp90)和热休克转录因子1(Hsf1)的状态。为了研究心肌Hsps的表达,雄性Wistar大鼠单次口服剂量为45和90?mg / kg F?。持续24小时使用RT-PCR,蛋白质印迹和免疫组化研究确定心肌Hsps的表达水平。与对照组相比,急性F2中毒的大鼠显示Hsf1,Hsp27,Hsp32,Hsp60和Hsp70的转录本和蛋白质表达水平升高。另外,在F 2处理的动物中,Hsp40和Hsp90的表达水平以剂量依赖性方式显着下降。我们的结果表明,大鼠心肌中Hsps的差异表达可以在急性F 2引起的心力衰竭期间作为促存活和死亡信号之间的平衡。

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