研究动态
Articles below are published ahead of final publication in an issue. Please cite articles in the following format: authors, (year), title, journal, DOI.

没食子酸通过人牙周膜细胞中的 GPR35/GSK3β/β-catenin 信号通路诱导成骨细胞分化并减轻炎症反应。

Gallic acid induces osteoblast differentiation and alleviates inflammatory response through GPR35/GSK3β/β-catenin signaling pathway in human periodontal ligament cells.

发表日期:2023 Nov 13
作者: Thi Hoa Pham, Eun-Nam Kim, Nguyen Minh Trang, Gil-Saeng Jeong
来源: JOURNAL OF PERIODONTAL RESEARCH

摘要:

没食子酸(GA)具有多种有益功能,包括抗氧化、抗癌、抗炎以及抑制破骨细胞生成。然而,对成骨分化的影响,特别是对人韧带牙周(hPDL)细胞的影响仍不清楚。因此,本研究的目的是评估GA对hPDL细胞成骨和抗炎的功能,并探讨其相关机制。牙龈卟啉单胞菌脂多糖(Pg-LPS)治疗被用作牙周炎模型。 ROS 的产生通过 H2DCFDA 染色测定。进行跨孔和伤口愈合试验以检查 GA 的迁移效果。进行茜素红和碱性磷酸酶活性(ALP)测定以评估成骨分化。通过实时PCR和蛋白质印迹测量成骨和炎症相关基因和蛋白质。我们的结果表明,GA处理的hPD​​L细胞具有更高的增殖和迁移效果。 GA 抑制 Pg-LPS 诱导的 ROS 产生。此外,GA 消除了 Pg-LPS 诱导的炎症细胞因子(il-6、il-1β)和炎症小体靶标(Caspase-1、NLRP3)。此外,GA促进hPDL细胞中的ALP活性和矿化,导致增强成骨细胞分化过程。 GA的作用与G蛋白偶联受体35(GPR35)/GSK3β/β-catenin信号通路有关。GA减弱Pg-LPS诱导的hPDL细胞炎症反应和牙周炎。综上所述,GA 可能成为牙周病治疗干预的目标。© 2023 John Wiley
Gallic acid (GA) possesses various beneficial functions including antioxidant, anticancer, anti-inflammatory as well as inhibiting osteoclastogeneis. However, effects on osteogenic differentiation, especially in human ligament periodontal (hPDL) cells, remain unclear. Thus, the aim of this study was to evaluate the function of GA on osteogenesis and anti-inflammation in hPDL cells and to explore the involved underlying mechanism.Porphyromonas gingivalis lipopolysaccharide (Pg-LPS) treatment was used as a model for periodontitis. ROS production was determined by H2DCFDA staining. Trans-well and wound healing assays were performed for checking the migration effect of GA. Alizarin red and alkaline phosphatase activity (ALP) assays were performed to evaluate osteogenic differentiation. Osteogenesis and inflammatory-related genes and proteins were measured by real-time PCR and western blot.Our results showed that GA-treated hPDL cells had higher proliferation and migration effect. GA inhibited ROS production-induced by Pg-LPS. Besides, GA abolished Pg-LPS-induced inflammation cytokines (il-6, il-1β) and inflammasome targets (Caspase-1, NLRP3). In addition, GA promoted ALP activity and mineralization in hPDL cells, lead to enhance osteoblast differentiation process. The effect of GA is related to G-protein-coupled receptor 35 (GPR35)/GSK3β/β-catenin signaling pathway.GA attenuated Pg-LPS-induced inflammatory responses and periodontitis in hPDL cells. Taken together, GA may be targeted for therapeutic interventions in periodontal diseases.© 2023 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.