Abstract
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.
Highlights
Periodontitis is characterized by an aberrant inflammatory response to oral commensal biofilms, resulting in destruction of periodontal tissues, especially in susceptible populations [1]
By combining network pharmacology analysis results and previous studies of other researchers on inflammatory diseases [9,10,11], we examined the effect of Rb3 on the mitogen-activated protein kinase (MAPK), AKT, and NF-kB pathways in P. gingivalis LPS-stimulated Human periodontal ligament cells (HPLCs)
We found that HPLCsHPLCs produced large amounts shorttime timeafter after stimulation, which was in accordance produced large amountsofofIL-8
Summary
Periodontitis is characterized by an aberrant inflammatory response to oral commensal biofilms, resulting in destruction of periodontal tissues, especially in susceptible populations [1]. Periodontitis is associated with a series of systemic diseases, such as endocarditis [2], cerebral vascular disease [3], and diabetes [4]. Porphyromonas gingivalis (P. gingivalis) is a major periodontal pathogenic bacterium. Its lipopolysaccharide (LPS) plays a crucial role in the pathogenesis of periodontitis by stimulating the host to secrete various pro-inflammatory mediators [5,6,7]. Human periodontal ligament cells (HPLCs), the main cellular constituents of the periodontium, secrete pro-inflammatory cytokines, such as interleukin (IL)-1β, IL-6, and IL-8, in response to pathogens, such as P. gingivalis [8]. The roles of nuclear factor-κB (NF-κB) and mitogen-activated protein kinase (MAPK) signaling pathways are well established in Molecules 2020, 25, 4815; doi:10.3390/molecules25204815 www.mdpi.com/journal/molecules
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