The heightened prevalence and accelerated progression of periodontitis in individuals with diabetes is primarily attributed to inflammatory responses in human periodontal ligament cells (HPDLCs). This study is aimed at delineating the regulatory mechanism of nucleotide-binding oligomerization domain-like receptors (NLRs) in mediating inflammation incited by muramyl dipeptide (MDP) in HPDLCs, under the influence of advanced glycation end products (AGEs), metabolic by-products associated with diabetes. We performed RNA-seq in HPDLCs induced by AGEs treatment and delineated activation markers for the receptor of AGEs (RAGE). It showed that advanced glycation end products modulate inflammatory responses in HPDLCs by activating NLRP1 and NLRP3 inflammasomes, which are further regulated through the NF-κB signaling pathway. Furthermore, AGEs synergize with NOD2, NLRP1, and NLRP3 inflammasomes to augment MDP-induced inflammation significantly.

中文翻译：

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AMPK/NF-κB/NLRP3信号通路调控AGEs诱导的人牙周膜细胞炎症反应

糖尿病患者牙周炎患病率的升高和进展的加速主要归因于人类牙周膜细胞（HPDLC）的炎症反应。本研究旨在阐明在晚期糖基化终末产物（AGEs）、代谢副产物的影响下，核苷酸结合寡聚化结构域样受体（NLRs）介导HPDLCs中胞壁酰二肽（MDP）引起的炎症的调节机制。与糖尿病有关。我们对 AGE 处理诱导的 HPDLC 进行了 RNA 测序，并描绘了 AGE 受体 (RAGE) 的激活标记。结果表明，晚期糖基化终末产物通过激活 NLRP1 和 NLRP3 炎症小体来调节 HPDLC 中的炎症反应，并通过 NF-κB 信号通路进一步调节。此外，AGEs 与 NOD2、NLRP1 和 NLRP3 炎症小体协同作用，显着增强 MDP 诱导的炎症。