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首页> 外文期刊>Cellular Signalling >Ephedrine induced thioredoxin-1 expression through β-adrenergic receptor/cyclic AMP/protein kinase A/dopamine- and cyclic AMP-regulated phosphoprotein signaling pathway
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Ephedrine induced thioredoxin-1 expression through β-adrenergic receptor/cyclic AMP/protein kinase A/dopamine- and cyclic AMP-regulated phosphoprotein signaling pathway

机译：麻黄碱通过β-肾上腺素受体/环AMP /蛋白激酶A /多巴胺和环AMP调节的磷蛋白信号通路诱导硫氧还蛋白-1表达

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摘要

Ephedrine (Eph) is one of alkaloids that has been isolated from the ancient herb ephedra (ma huang) and is used as the treatment of asthma, hypotension and fatigue. However, its molecular mechanism remains unknown. Thioredoxin-1 (Trx-1) is a redox regulating protein, which has various biological activities, including regulating transcription factor DNA binding activity and neuroprotection. In this study, we found that Eph induced Trx-1 expression, which was inhibited by propranolol (β-adrenergic receptor inhibitor), but not by phenoxybenzamine (α-adrenergic receptor inhibitor) in rat pheochromocytoma PC12 cells. Moreover, the increase of Trx-1 expression was inhibited by SQ22536 (adenylyl cyclase inhibitor) and H-89 (protein kinase A inhibitor). Interestingly, the effect of Eph on dopamine- and cyclic AMP-regulated phosphoprotein (DARPP-32) was similar to Trx-1. Thus, the relationship between Trx-1 and DARPP-32 was further studied. The DARPP-32 siRNA significantly reduced Trx-1 expression, but Trx-1 siRNA did not exchange DARPP-32. These results suggested that Eph induced the Trx-1 expression through β-adrenergic receptor/cyclic AMP/PKA/DARPP-32 signaling pathway. Furthermore, Eph induced PKA-mediated cyclic AMP response element-binding protein (CREB) phosphorylation. Down-regulation of DARPP-32 expression decreased phosphorylated CREB. In addition, Eph had a significant effect on the viability of the rat pheochromocytoma PC12 cells through β-adrenergic receptors. Trx-1 may play an important role in the actions of Eph.
机译：麻黄碱（Eph）是从古代草药麻黄中分离出的一种生物碱，被用于治疗哮喘，低血压和疲劳。但是，其分子机制仍然未知。硫氧还蛋白-1（Trx-1）是一种氧化还原调节蛋白，具有多种生物学活性，包括调节转录因子DNA结合活性和神经保护作用。在这项研究中，我们发现Eph诱导Trx-1表达，在大鼠嗜铬细胞瘤PC12细胞中，其被普萘洛尔（β-肾上腺素受体抑制剂）抑制，但不受苯氧基苯甲胺（α-肾上腺素受体抑制剂）抑制。此外，Trx-1表达的增加受到SQ22536（腺苷酸环化酶抑制剂）和H-89（蛋白激酶A抑制剂）的抑制。有趣的是，Eph对多巴胺和环状AMP调节的磷蛋白（DARPP-32）的作用类似于Trx-1。因此，进一步研究了Trx-1和DARPP-32之间的关系。 DARPP-32 siRNA显着降低了Trx-1的表达，但Trx-1 siRNA没有交换DARPP-32。这些结果表明，Eph通过β-肾上腺素受体/环AMP / PKA / DARPP-32信号通路诱导了Trx-1的表达。此外，Eph诱导PKA介导的环AMP响应元件结合蛋白（CREB）磷酸化。 DARPP-32表达的下调降低了磷酸化的CREB。此外，Eph通过β-肾上腺素能受体对大鼠嗜铬细胞瘤PC12细胞的生存能力具有重要影响。 Trx-1可能在Eph的行为中起重要作用。

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