Brain-derived neurotrophic factor (BDNF) is one of the neurotrophic factors that are vital to the survival and proliferation of neuron. Thioredoxin-1 (Trx-1) is a redox regulating protein and plays various roles in regulating transcript factors and inhibiting apoptosis. It has been reported that Trx-1 is required for nerve growth factor-mediated signal transduction and neurite outgrowth, and is involved in synaptic protein expression induced by BDNF. However, the molecular mechanism on BDNF inducing Trx-1 expression has not been fully verified. The present study investigated the expression of Trx-1 after treatment with BDNF in SH-SY5Y cells. We first demonstrated that cell viability and the expression of Trx-1 were increased by BDNF in SH-SY5Y cells, which were inhibited by the tyrosine kinase B (TrkB) inhibitor, K252a, and the phosphatidylinositol 3-kinase (PI3-K) inhibitor, LY294002. Moreover, BDNF increased the activity of cAMP response element-binding protein (CREB) through TrkB/PI3-K/Akt pathway. Whereas the expression of Trx-1 induced by BDNF was suppressed by CREB siRNA. Thus, our data suggest that BDNF induces the expression of Trx-1 through the TrkB/Akt/CREB pathway.

脑源性神经营养因子（BDNF）是对神经元的存活和增殖至关重要的神经营养因子之一。硫氧还蛋白-1（Trx-1）是一种氧化还原调节蛋白，在调节转录因子和抑制细胞凋亡中发挥多种作用。据报道，Trx-1是神经生长因子介导的信号转导和神经突向外生长所必需的，并参与BDNF诱导的突触蛋白表达。但是，BDNF诱导Trx-1表达的分子机制尚未得到充分证实。本研究调查了BDNF处理后Trx-1在SH-SY5Y细胞中的表达。我们首先证明BDNF在SH-SY5Y细胞中提高了细胞活力和Trx-1的表达，而酪氨酸激酶B（TrkB）抑制剂K252a抑制了该活性，磷脂酰肌醇3-激酶（PI3-K）抑制剂LY294002。此外，BDNF通过TrkB / PI3-K / Akt途径提高了cAMP反应元件结合蛋白（CREB）的活性。而BDNF诱导的Trx-1的表达被CREB ​​siRNA抑制。因此，我们的数据表明BDNF通过TrkB / Akt / CREB途径诱导Trx-1的表达。