Bisphenol A (BPA) is a typical environmental endocrine disruptor that can migrate into organisms through skin contact, breathing, diet and various other approaches. The reproductive toxicity and neurotoxicity of BPA has been confirmed by several toxicological studies. However, the neurotoxicity of BPA is still controversial. In the present study, we used PC12 cells as a model to investigate the mechanism of BPA-induced neuronal apoptosis. BPA exposure reduced cell viability, altered cell morphology and aggravated intracellular Lactate dehydrogenase (LDH) release, intracellular Ca²⁺ concentration, Reactive oxygen species (ROS) levels, apoptosis and the reduction in the mitochondrial transmembrane potential (ΔΨm). Moreover, the results of the Western blot (WB) and Real-time quantitative polymerase chain reaction (RT-qPCR) assays indicated that the expression levels of Nur77 in the BPA group were down-regulated and accompanied by the downregulation of the NF-κb/Bcl-2 proteins and the upregulation of cleaved-caspase 3, which is a marker of apoptosis. However, these changes were significantly reversed with the upregulation of the Nur77 protein by introducing plasmids carrying the nur77 gene. These results indicated that BPA-induced apoptosis was closely related to Nur77-mediated inhibition of the NF-κb/Bcl-2 pathway.

双酚A（BPA）是一种典型的环境内分泌干扰物，可以通过皮肤接触，呼吸，饮食和各种其他方式迁移到生物体内。BPA的生殖毒性和神经毒性已通过数项毒理学研究得到证实。然而，双酚A的神经毒性仍存在争议。在本研究中，我们使用PC12细胞作为模型来研究BPA诱导的神经元凋亡的机制。BPA暴露会降低细胞活力，改变细胞形态并加剧细胞内乳酸脱氢酶（LDH）释放，细胞内Ca ²⁺浓度，活性氧（ROS）水平，细胞凋亡和线粒体跨膜电位（ΔΨm）降低。此外，Western blot（WB）和实时定量聚合酶链反应（RT-qPCR）分析的结果表明，BPA组中Nur77的表达水平下调，并伴随着NF-κb的下调。 / Bcl-2蛋白和裂解半胱天冬酶3的上调，后者是细胞凋亡的标志。但是，通过引入携带nur77基因的质粒，Nur77蛋白的上调显着逆转了这些变化。这些结果表明，BPA诱导的凋亡与Nur77介导的NF-κb/ Bcl-2途径的抑制密切相关。