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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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摘要

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小时构建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阻止CREB激活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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