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Int J Rheum Dis ; 27(1): e14976, 2024 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-37997635

RESUMO

BACKGROUND: Rheumatoid arthritis (RA) is a kind of systemic autoimmune disease, and the joint inflammation and cartilage destruction are the major features. Some traditional Chinese medicine have been discovered to exhibit regulatory roles in the treatment of RA. Forsythiaside A (FA) as an active ingredient isolated from forsythia suspensa has been discovered to participate into the regulation of some diseases through improving inflammation. However, the regulatory effects of FA on the progression of RA keep indistinct. METHODS: IL-1ß treatment (10 ng/mL) in MH7A cells was built to mimic RA in vitro (cell) model. The cell viability was examined through CCK-8 assay. The cell proliferation was detected through Edu assay. The levels of TNF-α, IL-6, and IL-8 were evaluated through ELISA. The protein expressions were measured through western blot. The cell apoptosis was assessed through flow cytometry. The cell migration and invasion abilities were tested through Transwell assay. RESULTS: In this study, it was revealed that the cell proliferation was strengthened after IL-1ß treatment (p < .001), but this effect was reversed after FA treatment in a dose-increasing manner (p < .05). Furthermore, FA suppressed inflammation in IL-1ß-triggered MH7A cells through attenuating the levels of TNF-α, IL-6, and IL-8 (p < .05). The cell apoptosis was lessened after IL-1ß treatment (p < .001), but this effect was rescued after FA treatment (p < .05). Besides, the cell migration and invasion abilities were both increased after IL-1ß treatment (p < .001), but these changes were offset after FA treatment (p < .05). Eventually, FA retarded the JAK/STAT pathway through reducing p-JAK/JAK and p-STAT/STAT levels (p < .01). CONCLUSION: Our study manifested that FA exhibited anti-migration and anti-inflammation effects in RA in vitro model (IL-1ß-triggered MH7A cells) through regulating the JAK/STAT pathway. This work hinted that FA can be an effective drug for RA treatment.


Assuntos
Artrite Reumatoide , Glicosídeos , Fator de Necrose Tumoral alfa , Humanos , Fator de Necrose Tumoral alfa/farmacologia , Interleucina-6/metabolismo , Interleucina-8/metabolismo , Janus Quinases/metabolismo , Janus Quinases/farmacologia , Janus Quinases/uso terapêutico , Transdução de Sinais , Fatores de Transcrição STAT/metabolismo , Fatores de Transcrição STAT/farmacologia , Fatores de Transcrição STAT/uso terapêutico , Inflamação/metabolismo , Proliferação de Células , Fibroblastos/metabolismo
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