Thiamine-dependent processes are critical in cerebral glucose metabolism, it is abnormity induces oxidative stress, inflammation and neurodegeneration. Nod-like receptor protein-3 (NLRP3) inflammasome-mediated inflammation is closely related to neurologic diseases and can be activated by oxidative stress. However, the impact of thiamine deficiency on NLRP3 inflammasome activation remains unknown. In this study, we found that NLRP3 inflammasomes were significantly activated in the microglia of thiamine deficiency mice model. In contrast, benfotiamine dampened inflammation NLRP3 mediated in BV2 cells stimulated with LPS and ATP through reducing mitochondrial reactive oxygen species levels and mitigating autophagy flux defect. These data identify an important role of thiamine metabolism in NLRP3 inflammasome activation, and correcting thiamine metabolism through benfotiamine provides a new therapeutic strategy for NLRP3 inflammasome related neurological, metabolic, and inflammatory diseases.

中文翻译：

---

硫胺素缺乏和苯磷硫胺治疗对小胶质细胞中 Nod 样受体蛋白 3 炎性体的影响。

硫胺素依赖性过程在脑葡萄糖代谢中至关重要，它的异常会引起氧化应激、炎症和神经退行性变。Nod样受体蛋白3（NLRP3）炎症小体介导的炎症与神经系统疾病密切相关，并且可以被氧化应激激活。然而，硫胺素缺乏对 NLRP3 炎症小体激活的影响仍不清楚。在这项研究中，我们发现NLRP3炎症小体在硫胺素缺乏小鼠模型的小胶质细胞中显着激活。相比之下，苯磷硫胺通过降低线粒体活性氧水平和减轻自噬通量缺陷来抑制 LPS 和 ATP 刺激的 BV2 细胞中 NLRP3 介导的炎症。这些数据确定了硫胺素代谢在NLRP3炎症小体激活中的重要作用，通过苯磷硫胺纠正硫胺素代谢为NLRP3炎症小体相关的神经、代谢和炎症疾病提供了新的治疗策略。