NLRP3炎症小体异常活化诱发的炎症反应会导致多种人类重大疾病的发生，如二型糖尿病、阿尔兹海默症、痛风、肿瘤等，因此机体必然存在严格的调控机制抑制炎症小体的过度活化，但到目前为止，其负调控机制还需进一步研究。维生素K作为一种脂溶性的维生素,在抗凝血过程中有重要作用，但在免疫和炎症的调控过程中作用机制还不清楚。我们前期预实验结果发现，维生素K能够特异性地抑制NLRP3炎症小体的活化，但对AIM2和IPAF炎症小体的活化并没有影响。我们以此为基础，一方面将深入研究维生素K负调炎症小体活化的细胞分子机制以及信号通路，另一方面利用阿尔兹海默症和MSU腹膜炎两种动物模型来探究维生素K是否通过抑制炎症小体的活化从而改善疾病的发生进程。该项研究不仅有助于认识维生素K的抗炎新功能及其作用机制，还能为阐明炎症小体活化的负调控机制及胞内调控网络提供线索。

NLRP3 inflammsome plays an important role in many human major diseases, such as diabetes, Alzheimer disease, gout and tumor, this suggests that there must be a very strict negative regulation mechanism to avoid excessive activation of NLRP3 inflammsome. However, so far, the negative regulation network of the activation of NLRP3 inflammsome is still unclear, further research is needed. Our results showed that vitamin K could specifically inhibit the activation of NLRP3 inflammasome, but had no effect on the activation of AIM2 and IPAF inflammasome. Taking these as the foundation, on the one hand we will further investigate the inhibitory role of Vitamin K in inflammasome activation and the potential cellular and molecular mechanisms, on the other hand we will use Alzheimer's disease animal model and MSU peritonitis animal model to explore whether Vitamin K can improve the progression of diseases through inhibiting the activation of inflammasome. This study is helpful to understand the anti-inflammatory mechanisms of new functions of Vitamin K and also will provide new clues to clarify the mechanisms and negatiye regulatory network of inflammasome activation.