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The expression of thioredoxin-1 in acute epinephrine stressed mice

机译:硫氧还蛋白-1在急性肾上腺素应激小鼠中的表达

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Stress, a state of perceived threat to homeostasis, regulates a panel of important physiological functions. The human mind and body respond to stress by activating the sympathetic nervous system and secreting the catecholamines epinephrine and norepinephrine in the “fight-or-flight” response. However, the protective mechanism of acute stress is still unknown. In the present study, an acute stress mouse model was constructed by intraperitoneal injection of epinephrine (0.2?mg?kg?1) for 4?h. Epinephrine treatment induced heat shock 70(Hsp70) expression in the stress responsive tissues, such as the cortex, hippocampus, thymus, and kidney. Further, the expression of thioredoxin-1(Trx-1), a cytoprotective protein, was also upregulated in these stress responsive tissues. In addition, the phosphorylation of cAMP-response element binding protein (CREB), a transcription factor of Trx-1, was increased after treatment with epinephrine. The block of CREB activation by H89 inhibited the acute epinephrine stress-induced Trx-1 and Hsp70 expression. Taken together, our data suggest that acute stimuli of epinephrine induced Trx-1 expression through activating CREB and may represent a protective role against stress.
机译:压力是对稳态的一种感知威胁,它调节着一系列重要的生理功能。人类的思想和身体通过激活交感神经系统并在“战斗或逃跑”反应中分泌儿茶酚胺肾上腺素和去甲肾上腺素来应对压力。但是,急性应激的保护机制仍是未知的。在本研究中,通过腹膜内注射肾上腺素(0.2?mg?kg?1)4?h建立了急性应激小鼠模型。肾上腺素治疗诱导应激反应的组织,如皮质,海马,胸腺和肾脏中的热休克70(Hsp70)表达。此外,硫氧还蛋白-1(Trx-1),一种细胞保护蛋白,在这些应激反应组织中的表达也被上调。此外,用肾上腺素治疗后,cAMP反应元件结合蛋白(CREB)(Trx-1的转录因子)的磷酸化增加。 H89激活CREB的阻滞抑制了急性肾上腺素应激诱导的Trx-1和Hsp70表达。两者合计,我们的数据表明肾上腺素的急性刺激通过激活CREB诱导Trx-1表达,并可能代表抗压力的保护作用。

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