Phytomedicine : international journal of phytotherapy and phytopharmacology · 2026
Sinomenine treats Rheumatoid Arthritis by regulating IL-6 Gene Promoter Methylation.
СтатьяНазвание и аннотация: Перевод в очереди
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.
Luo Jin-Fang, Yu Yang, Yao Yun-Da, Zhang Cui, Liu Jian-Xin, Lio Chonkit, Qian Hai-Bing, Zhou Hua
Аннотация
BACKGROUND: Sinomenine (SIN) is the main active component of the Chinese herbal medicine Sinomenium acutum (Thunb.) Rehder & E.H.Wilson. It exerts therapeutic effects on rheumatoid arthritis (RA), but its underlying mechanism remains incompletely understood.
PURPOSE: This study explored the mechanism of SIN's anti-inflammatory and anti-RA effects by modulating the interleukin-6 (IL-6) gene promoter methylation, using integrated network pharmacology and experimental analysis.
MATERIALS AND METHODS: Network pharmacology and bioinformatics identified core targets and signaling pathways of SIN against RA. Molecular docking confirmed binding potential of SIN to core targets. Inflammatory models were established in LPS-stimulated RAW264.7 and THP-1 cells; CCK-8 assay, NO/cytokine (TNF-α, IL-6) detection, Western blot (DNMT1, DNMT3b, p-STAT3, p-JAK2), and bisulfite sequencing (IL-6 promoter methylation in THP-1 cells) were performed. A collagen-induced arthritis (CIA) rat model evaluated in vivo efficacy via foot swelling, arthritis index, cytokine levels, and histological analysis.
RESULTS: SIN targets TNF-α, IL-1β, IL-6, STAT3, PTGS2, JAK2 mainly via the JAK-STAT pathway. In vitro, SIN reduced LPS-induced NO/TNF-α/IL-6, upregulated IL-6 promoter methylation (reversed by 5-Aza). In vivo, SIN alleviated CIA rats' paw edema, arthritis index, synovial inflammation, and lowered TNF-α/IL-6.
CONCLUSIONS: SIN alleviates inflammation and RA progression by enhancing IL-6 promoter specific site methylation levels, modulating inflammatory responses via epigenetic regulation.
PURPOSE: This study explored the mechanism of SIN's anti-inflammatory and anti-RA effects by modulating the interleukin-6 (IL-6) gene promoter methylation, using integrated network pharmacology and experimental analysis.
MATERIALS AND METHODS: Network pharmacology and bioinformatics identified core targets and signaling pathways of SIN against RA. Molecular docking confirmed binding potential of SIN to core targets. Inflammatory models were established in LPS-stimulated RAW264.7 and THP-1 cells; CCK-8 assay, NO/cytokine (TNF-α, IL-6) detection, Western blot (DNMT1, DNMT3b, p-STAT3, p-JAK2), and bisulfite sequencing (IL-6 promoter methylation in THP-1 cells) were performed. A collagen-induced arthritis (CIA) rat model evaluated in vivo efficacy via foot swelling, arthritis index, cytokine levels, and histological analysis.
RESULTS: SIN targets TNF-α, IL-1β, IL-6, STAT3, PTGS2, JAK2 mainly via the JAK-STAT pathway. In vitro, SIN reduced LPS-induced NO/TNF-α/IL-6, upregulated IL-6 promoter methylation (reversed by 5-Aza). In vivo, SIN alleviated CIA rats' paw edema, arthritis index, synovial inflammation, and lowered TNF-α/IL-6.
CONCLUSIONS: SIN alleviates inflammation and RA progression by enhancing IL-6 promoter specific site methylation levels, modulating inflammatory responses via epigenetic regulation.
Предметные рубрики MeSH
AnimalsMorphinansInterleukin-6Promoter Regions, GeneticArthritis, RheumatoidHumansMiceDNA MethylationRAW 264.7 CellsRatsArthritis, ExperimentalMolecular Docking SimulationAnti-Inflammatory AgentsMaleTHP-1 CellsRats, Sprague-DawleyNetwork PharmacologySignal TransductionSinomeniumTumor Necrosis Factor-alpha