Mental stress has been shown to activate sympathetic adrenergic system to produce dopamine and finally promote the progression of cancer. Dopamine can also regulate the immune system through secreting kinds of cytokines. However, what role does dopamine play in acute myeloid leukemia (AML) remains unclear. Here, we investigated the effects and mechanisms of dopamine in NLRP3 inflammasome activation and cellular viability of acute myeloid leukemia U937 cells. Our results showed that dopamine enhanced the viability of U937 cells and activated the NLRP3 inflammasome in U937 cells. To further explore the mechanism of dopamine on U937 cells, we examined the expression level of dopamine receptors (DRs). We found that the mRNA expression level of DR5 in U937 cells was significantly higher than other dopamine receptors. Furthermore, we treated U937 cells with DR1/2/3/5 antagonist before dopamine, and it manifestly reversed the NLRP3 inflammasome activation and the viability-enhancing effect in U937 cells induced by dopamine. Anti-IL-1β antibody also could partly reversed the viability-enhancing effect by dopamine. We concluded that dopamine could enhance the viability of U937 cells through DR1/5 receptor pathway and activate NLRP3 inflammasome.

精神压力已被证明会激活交感神经肾上腺素能系统以产生多巴胺并最终促进癌症的进展。多巴胺还可以通过分泌多种细胞因子来调节免疫系统。然而，多巴胺在急性髓性白血病 (AML) 中的作用仍不清楚。在这里，我们研究了多巴胺在急性髓细胞白血病 U937 细胞的 NLRP3 炎性体激活和细胞活力中的作用和机制。我们的研究结果表明，多巴胺增强了 U937 细胞的活力并激活了 U937 细胞中的 NLRP3 炎性体。为了进一步探索多巴胺对 U937 细胞的作用机制，我们检测了多巴胺受体 (DR) 的表达水平。我们发现 U937 细胞中 DR5 的 mRNA 表达水平显着高于其他多巴胺受体。此外，我们在多巴胺之前用 DR1/2/3/5 拮抗剂处理 U937 细胞，它明显逆转了多巴胺诱导的 NLRP3 炎性体激活和 U937 细胞的活力增强作用。抗 IL-1β 抗体也可以部分逆转多巴胺的活力增强作用。我们得出结论，多巴胺可以通过 DR1/5 受体途径增强 U937 细胞的活力并激活 NLRP3 炎性体。