Ginsenoside Rb3 Inhibits Pro-Inflammatory Cytokines via MAPK/AKT/NF-κB Pathways and Attenuates Rat Alveolar Bone Resorption in Response to Porphyromonas gingivalis LPS.
Ginsenoside Rb3 Inhibits Pro-Inflammatory Cytokines via MAPK/AKT/NF-κB Pathways and Attenuates Rat Alveolar Bone Resorption in Response to Porphyromonas gingivalis LPS.
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人参皂苷 Rb3 通过 MAPK/AKT/NF-κB 途径抑制促炎细胞因子，并减弱大鼠牙槽骨吸收以响应牙龈卟啉单胞菌 LPS
DOI：
10.3390/molecules25204815
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发表时间：
2020-10-20
期刊：
影响因子：
--
通讯作者：
Du M
中科院分区：
文献类型：
--
作者：
Sun M;Ji Y;Li Z;Chen R;Zhou S;Liu C;Du M
慢性牙周炎的传统治疗方法在控制炎症方面效果较差，并且经常复发。因此，有必要探索免疫调节药物作为辅助治疗。人参皂苷Rb 3（Rb 3）是人参中含量最丰富的活性成分之一，具有抗炎和免疫调节作用。本研究首次检测了Rb 3对牙龈卟啉单胞菌LPS刺激的人牙周膜细胞和实验性牙周炎大鼠的抗炎作用。我们发现，前炎症介质，包括IL-1β，IL-6和IL-8的表达，由脂多糖（LPS）刺激上调显着下调Rb 3治疗剂量依赖性的方式在转录和翻译水平。Rb 3的网络药理学分析表明，丝裂原活化蛋白激酶（MAPK）信号通路具有最高的丰富性，p38，JNK和ERK分子是Rb 3在人体内的潜在靶点。Western blot结果显示Rb 3能显著抑制p38 MAPK和p65 NF-κB的磷酸化，并降低AKT的表达。在实验性牙周炎大鼠模型中，观察到Rb 3治疗组的牙槽骨吸收和破骨细胞生成减少。因此，Rb 3可通过抑制MAPK/AKT/NF-κB信号通路减轻牙龈卟啉单胞菌LPS诱导的炎症反应，减轻牙周炎大鼠牙槽骨吸收。
Conventional treatments for chronic periodontitis are less effective in controlling inflammation and often relapse. Therefore, it is necessary to explore an immunomodulatory medication as an adjuvant. Ginsenoside Rb3 (Rb3), one of the most abundant active components of ginseng, has been found to possess anti-inflammatory and immunomodulatory properties. Here, we detected the anti-inflammatory effect of Rb3 on Porphyromonas gingivalis LPS-stimulated human periodontal ligament cells and experimental periodontitis rats for the first time. We found that the expression of pro-inflammatory mediators, including IL-1β, IL-6 and IL-8, upregulated by lipopolysaccharide (LPS) stimulation was remarkably downregulated by Rb3 treatment in a dose-dependent manner at both transcriptional and translational levels. Network pharmacological analysis of Rb3 showed that the mitogen-activated protein kinase (MAPK) signaling pathway had the highest richness and that p38, JNK, and ERK molecules were potential targets of Rb3 in humans. Western blot analysis revealed that Rb3 significantly suppressed the phosphorylation of p38 MAPK and p65 NF-κB, as well as decreased the expression of total AKT. In experimental periodontitis rat models, reductions in alveolar bone resorption and osteoclast generation were observed in the Rb3 treatment group. Thus, we can conclude that Rb3 ameliorated Porphyromonas gingivalis LPS-induced inflammation by inhibiting the MAPK/AKT/NF-κB signaling pathways and attenuated alveolar bone resorption in experimental periodontitis rats.
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