动脉粥样硬化是一种慢性炎症性疾病。巨噬细胞中NLRP3炎性体的激活导致白细胞介素-1β(IL-1β)分泌，在动脉粥样硬化形成过程中起极其重要的作用。作为炎性体的核心成分NLRP3蛋白的上调是炎性体激活启动的首要条件,但是，其上调的机制尚不清楚。我们前期结果发现：miR-223表达水平在ApoE-/-小鼠的动脉病变组织中显著下调,生物信息学预测提示NLRP3为miR-223的靶基因。我们还发现,在人巨噬细胞系THP-1细胞中导入miR-223能抑制IL-1β分泌。由此提出miR-223调控NLRP3表达进而抑制IL-1β分泌的假设。本项目拟进一步证实NLRP3是否为miR-223的直接靶基因，miR-223参与抑制IL-1β分泌是否影响动脉粥样硬化病变过程中炎症程度，在细胞水平和动物模型层面深入探讨miR-223抗动脉粥样硬化炎症发展的作用机理，为动脉粥样硬化早期诊断和治疗提供新的理论依据。

Atherosclerosis has been described as a chronic in?ammatory disease. Activation of the NLRP3 inflammasome located in macrophage, which induces secretion of IL-1β plays important role in atherosclerosis. NLRP3 up regulation is the first step of NLRP3 inflammasome activation. However, the mechanism of this procedure is still unknown. Our initial research found that miR-223 down regulated in atheromatous plaque in ApoE-/- mouse in late stage of atherosclerosis. Bioinformatics analysis indicated that NLRP3 may be the target gene of miR-223. Further study confirmed that overexpression of miR-223 in THP-1 cell can inhibit the secretion of IL-1β. So,We raise a hypothesis that miR-223 inhibite the secretion of IL-1β via downregulation of NLRP3 post-transcriptionally.Next, we will verify that whether the NLRP3 is the direct target gene of miR-223 and whether IL-1β inhibited by miR-223 can prevent inflammation in atherosclerosis. The mechanism of miR-223 inhibiting inflammation in atherosclerosis will be investigated in vivo and vitro. With these effort, we can provide some new ideas and targets for the treatment of atherosclerosis.