Exposure to organic solvents is associated with various health problems, including neurodegenerative diseases. Among these solvents, 1,2-diethylbenzene is notable for its ability to produce a toxic metabolite, 1,2-Diacetylbenzene (DAB), which can cause memory impairment. Prolactin (PRL) is theorized to protect the central nervous system. Certain antipsychotic drugs, known for increasing PRL secretion, have shown to improve cognitive performance in psychotic Alzheimer's patients. Among these, amisulpride stands out for its high efficacy, limited side effects, and high selectivity for dopamine D2 receptors. In our study, we explored the potential of amisulpride to inhibit DAB-induced neurotoxicity via PRL activation. Our results show that amisulpride enhances the PRL/JAK/STAT, PI3K/AKT, and BDNF/ERK/CREB pathways, playing critical roles in PRL’s neuroprotection pathways and memory formation. Additionally, amisulpride inhibited DAB-triggered NLRP3 inflammasome activation and apoptosis. Collectively, these findings suggest that amisulpride may be a promising therapeutic intervention for DAB-induced neurotoxicity, partly through activating the PRL pathway.

中文翻译：

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催乳素在氨磺必利对1,2-二乙酰苯神经毒性保护作用中的作用

接触有机溶剂与各种健康问题有关，包括神经退行性疾病。在这些溶剂中，1,2-二乙苯以其产生有毒代谢物 1,2-二乙酰苯 (DAB) 的能力而闻名，这种代谢物会导致记忆障碍。催乳素 (PRL) 理论上可以保护中枢神经系统。某些以增加 PRL 分泌而闻名的抗精神病药物已被证明可以改善精神病性阿尔茨海默病患者的认知能力。其中，氨磺必利因其疗效高、副作用小以及对多巴胺D2受体的高选择性而脱颖而出。在我们的研究中，我们探索了氨磺必利通过 PRL 激活抑制 DAB 诱导的神经毒性的潜力。我们的结果表明，氨磺必利增强 PRL/JAK/STAT、PI3K/AKT 和 BDNF/ERK/CREB ​​通路，在 PRL 的神经保护通路和记忆形成中发挥关键作用。此外，氨磺必利还能抑制 DAB 触发的 NLRP3 炎症小体激活和细胞凋亡。总的来说，这些研究结果表明，氨磺必利可能是治疗 DAB 诱导的神经毒性的一种有前途的治疗干预措施，部分是通过激活 PRL 途径实现的。