MicroRNA functions as an important part of the activity and development of immune cells. miR-499 has been demonstrated to play a significant role in the activity and development of immune cells. The precise mechanism by which miR-499 regulates the inflammatory response, however, remains unclear. This study was aimed to examine the role of microRNA miR-499 in the regulation of the inflammatory response in macrophages. RAW 264.7 macrophages were used as a cell model. The levels of miR-499 were measured in Porphyromonas gingivalis LPS-stimulated macrophages using qRT-PCR, and the levels of inflammatory cytokines (IL-6, IL-1β, and TNF-α) were determined using both qRT-PCR and ELISA. StarBase was used to predict the binding sites between NRIP1 and miR-499, and the mRNA expression of NRIP1 was measured using qRT-PCR. The regulation of inflammatory factors controlled by miR-499 was also evaluated by using miR-499 inhibitor and sh-NRIP1. The activation of the JAK/STAT pathway was determined using western blotting to measure the levels of phosphorylated JAK2 and STAT1. Porphyromonas gingivalis LPS caused a high expression of miR-499, which promoted the inflammatory response in macrophages. miR-499 targeted the NRIP1 3′UTR and regulated the mRNA expression of inflammatory cytokines, including IL-6, IL-1β, and TNF-α. The positive correlation between miR-499 and the expression of inflammatory factors and the negative correlation between NRIP1 and miR-499 suggests that the regulation of inflammatory factors controlled by miR-499 was associated with NRIP1. The phosphorylated proteins of the JAK/STAT pathway (p-JAK2 and p-STAT1) were activated by miR-499 through its regulation of NRIP1. These findings suggest that miR-499 regulates the P. gingivalis LPS-induced inflammatory response in macrophages and activates the JAK/STAT pathway through the regulation of NRIP1.

MicroRNA 是免疫细胞活动和发育的重要组成部分。miR-499 已被证明在免疫细胞的活性和发育中发挥重要作用。然而，miR-499 调节炎症反应的确切机制仍不清楚。本研究旨在探讨 microRNA miR-499 在调节巨噬细胞炎症反应中的作用。使用 RAW 264.7 巨噬细胞作为细胞模型。使用 qRT-PCR 测量牙龈卟啉单胞菌LPS 刺激的巨噬细胞中 miR-499 的水平，并使用 qRT-PCR 和 ELISA 测定炎症细胞因子（IL-6、IL-1β 和 TNF-α）的水平。使用StarBase预测NRIP1和miR-499之间的结合位点，并使用qRT-PCR测量NRIP1的mRNA表达。还使用 miR-499 抑制剂和 sh-NRIP1 评估了 miR-499 控制的炎症因子的调节。使用蛋白质印迹法测量磷酸化 JAK2 和 STAT1 的水平来确定 JAK/STAT 通路的激活。牙龈卟啉单胞菌LPS 引起 miR-499 高表达，促进巨噬细胞炎症反应。miR-499靶向NRIP1 3'UTR并调节炎性细胞因子的mRNA表达，包括IL-6、IL-1β和TNF-α。miR-499与炎症因子表达呈正相关，NRIP1与miR-499呈负相关，提示miR-499对炎症因子的调控与NRIP1相关。JAK/STAT 通路的磷酸化蛋白（p-JAK2 和 p-STAT1）由 miR-499 通过其对 NRIP1 的调节而激活。这些发现表明，miR-499 调节巨噬细胞中牙龈卟啉单胞菌 LPS 诱导的炎症反应，并通过调节 NRIP1 激活 JAK/STAT 通路。