Ginsenoside Rb3 alleviates the formation of osteoclasts induced by periodontal ligament fibroblasts in the periodontitis microenvironment through the STAT3 pathway

IF 3.3 3区 生物学 Q3 CELL BIOLOGY
Yuhua Zhang, Hanping Shi
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引用次数: 0

Abstract

This study explores the potential role and mechanism of Ginsenoside Rb3 (Rb3) in modulating osteoclastogenesis induced by human periodontal ligament fibroblasts (hPLFs) within the periodontitis microenvironment. We investigated the anti-inflammatory effects of Rb3 on hPLFs stimulated with Porphyromonas gingivalis lipopolysaccharide (P.g-LPS) utilizing quantitative polymerase chain reaction (qPCR) and enzyme-linked immunosorbent assay techniques. Moreover, the functional role of Rb3 in hPLFs-induced osteoclast formation was assessed by treating human bone marrow-derived macrophages (hBMMs) with conditioned medium from hPLFs, followed by analyses through qPCR, western blot analysis, and staining for tartrate-resistant acid phosphatase (TRAP) and phalloidin. The impact of Rb3 on the activation of the STAT3 signaling pathway was determined via western blot analysis. Results indicated that Rb3 treatment significantly suppressed the upregulation of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6, MCP-1, and IL-18) at both gene and protein levels in hPLFs induced by P.g-LPS. Furthermore, conditioned medium from Rb3 plus P.g-LPS treated hPLFs notably decreased the number of TRAP-positive cells, actin ring formations, and the expression of osteoclast marker genes (including CTSK, NFATC1, and ACP5). Rb3 also inhibited the P.g-LPS-induced activation of the STAT3 pathway, with the activation of STAT3 partially reversing the effects of Rb3 on inflammation and osteoclast differentiation. Collectively, Rb3 ameliorates inflammation in P.g-LPS-stimulated hPLFs and reduces hPLFs-induced osteoclastogenesis by inhibiting the STAT3 signaling pathway, suggesting its potential as a therapeutic agent for periodontitis.

人参皂苷 Rb3 可通过 STAT3 通路缓解牙周炎微环境中牙周韧带成纤维细胞诱导的破骨细胞的形成。
本研究探讨了人参皂苷 Rb3(Rb3)在牙周炎微环境中调节人牙周韧带成纤维细胞(hPLFs)诱导的破骨细胞生成过程中的潜在作用和机制。我们利用定量聚合酶链反应(qPCR)和酶联免疫吸附试验技术研究了 Rb3 对牙龈卟啉菌脂多糖(P.g-LPS)刺激的 hPLFs 的抗炎作用。此外,Rb3在hPLFs诱导的破骨细胞形成中的功能作用是通过用hPLFs的条件培养基处理人骨髓源性巨噬细胞(hBMMs),然后通过qPCR、Western印迹分析以及耐酒石酸磷酸酶(TRAP)和类磷青染色来评估的。Rb3 对 STAT3 信号通路活化的影响是通过 Western 印迹分析确定的。结果表明,Rb3处理能在基因和蛋白水平上显著抑制P.g-LPS诱导的hPLF中促炎细胞因子(TNF-α、IL-1β、IL-6、MCP-1和IL-18)的上调。此外,Rb3 加 P.g-LPS 处理 hPLFs 的条件培养基显著减少了 TRAP 阳性细胞的数量、肌动蛋白环的形成以及破骨细胞标记基因(包括 CTSK、NFATC1 和 ACP5)的表达。Rb3 还能抑制 P.g-LPS 诱导的 STAT3 通路的激活,STAT3 的激活能部分逆转 Rb3 对炎症和破骨细胞分化的影响。总之,Rb3通过抑制STAT3信号通路,改善了P.g-LPS刺激的hPLFs的炎症反应,并减少了hPLFs诱导的破骨细胞生成,这表明它有可能成为牙周炎的一种治疗药物。
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来源期刊
Cell Biology International
Cell Biology International 生物-细胞生物学
CiteScore
7.60
自引率
0.00%
发文量
208
审稿时长
1 months
期刊介绍: Each month, the journal publishes easy-to-assimilate, up-to-the minute reports of experimental findings by researchers using a wide range of the latest techniques. Promoting the aims of cell biologists worldwide, papers reporting on structure and function - especially where they relate to the physiology of the whole cell - are strongly encouraged. Molecular biology is welcome, as long as articles report findings that are seen in the wider context of cell biology. In covering all areas of the cell, the journal is both appealing and accessible to a broad audience. Authors whose papers do not appeal to cell biologists in general because their topic is too specialized (e.g. infectious microbes, protozoology) are recommended to send them to more relevant journals. Papers reporting whole animal studies or work more suited to a medical journal, e.g. histopathological studies or clinical immunology, are unlikely to be accepted, unless they are fully focused on some important cellular aspect. These last remarks extend particularly to papers on cancer. Unless firmly based on some deeper cellular or molecular biological principle, papers that are highly specialized in this field, with limited appeal to cell biologists at large, should be directed towards journals devoted to cancer, there being very many from which to choose.
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