Prolactin-releasing peptide (PrRP) has been investigated as a potential therapeutic for diabetes by the effect of food intake reduction, increasing leptin signaling, and insulin tolerance. Recent studies focused on its synaptogenesis and protective effects against neurodegeneration. Whereas 1,2-diacetylbenzene (DAB), a common metabolite of a neurotoxicant 1,2-diethyl benzene, causes memory impairment and neurotoxicity partly through the inflammatory process. Our present study assessed the effect of PrRP in microglia and its action in balancing the inflammation to protect against DAB. We observed that PrRP modulated NADPH oxidase - regulated NLRP3 inflammasome and PRL signaling pathways differently between physical and toxic conditions in microglia.

催乳素释放肽 (PrRP) 通过减少食物摄入、增加瘦素信号传导和胰岛素耐受性而被研究为糖尿病的潜在治疗方法。最近的研究重点是其突触发生和对神经退行性变的保护作用。而 1,2-二乙酰苯 (DAB) 是神经毒剂 1,2-二乙苯的常见代谢物，部分通过炎症过程导致记忆障碍和神经毒性。我们目前的研究评估了 PrRP 在小胶质细胞中的作用及其平衡炎症以预防 DAB 的作用。我们观察到，在小胶质细胞的物理条件和毒性条件下，PrRP 调节 NADPH 氧化酶、调节 NLRP3 炎性体和 PRL 信号通路的方式不同。