Frontiers in pharmacology · 2026
Pimpinella brachycarpa extract attenuates periodontal inflammation by modulating the PI3K/Akt-NF-κB signaling pathway.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Lee A Yeong, Park Su-Bin, Son Eunjung, Kim Junghyun, Kim Dong-Seon, Park Soon Yeong, Ku Hyeri, Kim Jung-In, Lee Yun Mi
Аннотация
INTRODUCTION: This study was conducted to investigate the preventive effects of Pimpinella brachycarpa extract (PBE), which has demonstrated anti-inflammatory effects but whose molecular mechanisms and active components are not completely understood, in experimental periodontitis and to elucidate its underlying mechanisms.
METHODS: The protective effects of PBE were evaluated in a lipopolysaccharide (LPS)-induced periodontitis rat model by assessing histological changes, TRAP-positive osteoclast presence, and alveolar bone loss. Network pharmacology, protein-protein interaction network analysis, KEGG pathway enrichment analysis, and molecular docking were performed to predict the potential targets and mechanisms of PBE. The anti-inflammatory effects of PBE were further investigated in RAW264.7 macrophages and human periodontal ligament fibroblasts (PDLFs). Inflammatory mediators, cytokines, matrix metalloproteinases (MMPs), and PI3K/Akt/NF-κB signaling-related proteins were analyzed. Major constituents of PBE were identified using UPLC-QTOF-MS, and their anti-inflammatory activities were evaluated in vitro.
RESULTS: PBE attenuated periodontal tissue destruction in LPS-induced periodontitis rats, as demonstrated by reduced inflammatory cell infiltration, decreased CEJ-ABC distance, and suppression of TRAP-positive osteoclast presence. Network pharmacology analysis identified the PI3K/Akt signaling pathway as a key target associated with the anti-inflammatory effects of PBE. In RAW264.7 macrophages, PBE significantly reduced the production of NO, PGE2, TNF-α, and IL-1β. In PDLFs, PBE suppressed IL-1β-induced production of PGE2, IL-6, and IL-1β and downregulated the expression of MMP-3, MMP-8, and MMP-13. Furthermore, PBE inhibited the phosphorylation of PI3K, Akt, IKK, IκBα, and NF-κB p65. Chemical profiling identified chlorogenic acid, luteolin 7-O-glucuronide, apigenin 7-O-glucuronide, and luteolin 3'-O-glucuronide as major constituents. Among these, flavonoid glucuronides exhibited stronger anti-inflammatory activities than chlorogenic acid in vitro.
CONCLUSION: The present findings indicate that PBE exerts anti-inflammatory and tissue-protective effects in experimental models of periodontitis. The observed effects were associated with suppression of PI3K/Akt-NF-κB signaling. In addition, flavonoid glucuronides identified in PBE exhibited anti-inflammatory activities in vitro. Further studies are required to clarify the contribution of individual constituents to the biological activity of PBE.
METHODS: The protective effects of PBE were evaluated in a lipopolysaccharide (LPS)-induced periodontitis rat model by assessing histological changes, TRAP-positive osteoclast presence, and alveolar bone loss. Network pharmacology, protein-protein interaction network analysis, KEGG pathway enrichment analysis, and molecular docking were performed to predict the potential targets and mechanisms of PBE. The anti-inflammatory effects of PBE were further investigated in RAW264.7 macrophages and human periodontal ligament fibroblasts (PDLFs). Inflammatory mediators, cytokines, matrix metalloproteinases (MMPs), and PI3K/Akt/NF-κB signaling-related proteins were analyzed. Major constituents of PBE were identified using UPLC-QTOF-MS, and their anti-inflammatory activities were evaluated in vitro.
RESULTS: PBE attenuated periodontal tissue destruction in LPS-induced periodontitis rats, as demonstrated by reduced inflammatory cell infiltration, decreased CEJ-ABC distance, and suppression of TRAP-positive osteoclast presence. Network pharmacology analysis identified the PI3K/Akt signaling pathway as a key target associated with the anti-inflammatory effects of PBE. In RAW264.7 macrophages, PBE significantly reduced the production of NO, PGE2, TNF-α, and IL-1β. In PDLFs, PBE suppressed IL-1β-induced production of PGE2, IL-6, and IL-1β and downregulated the expression of MMP-3, MMP-8, and MMP-13. Furthermore, PBE inhibited the phosphorylation of PI3K, Akt, IKK, IκBα, and NF-κB p65. Chemical profiling identified chlorogenic acid, luteolin 7-O-glucuronide, apigenin 7-O-glucuronide, and luteolin 3'-O-glucuronide as major constituents. Among these, flavonoid glucuronides exhibited stronger anti-inflammatory activities than chlorogenic acid in vitro.
CONCLUSION: The present findings indicate that PBE exerts anti-inflammatory and tissue-protective effects in experimental models of periodontitis. The observed effects were associated with suppression of PI3K/Akt-NF-κB signaling. In addition, flavonoid glucuronides identified in PBE exhibited anti-inflammatory activities in vitro. Further studies are required to clarify the contribution of individual constituents to the biological activity of PBE.