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Biosci Trends ; 18(2): 187-194, 2024 Jun 06.
Artículo en Inglés | MEDLINE | ID: mdl-38599880

RESUMEN

Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by chronic and symmetric in-flammation. Our previous research revealed an imbalance in the gut flora of RA patients and showed that certain gut microbiota can accelerate RA progression by enhancing vitamin C degradation. However, it is unclear whether vitamin C supplementation could improve the gut microbiota to prevent the development of arthritis by interfering with the gut-joint axis. In this work, we aimed to evaluate the effects of vitamin C in regulating the gut microbiota and to elucidate its potential role in the onset and progression of RA in a mouse model, thus providing a basis for the development of new intervention strategies and treatments for RA. In this study, collagen-induced arthritis (CIA) mouse models, biochemical, histological and 16S rRNA microbiological methods were used to investigate the role and possible mechanism of vitamin C in rheumatoid arthritis. The results showed that treatment of CIA mice with vitamin C effectively rescued the gut mi-crobiota imbalance and suppressed the inflammatory response associated with RA, and effectively alleviated arthritis symptoms in mice in which levels of the pro-inflammatory cytokines IL-6 and TNF-α were specifi-cally reduced. In conclusion, our results demonstrate the potential of vitamin C as a potential therapeutic choice for RA.


Asunto(s)
Artritis Experimental , Artritis Reumatoide , Ácido Ascórbico , Microbioma Gastrointestinal , Animales , Ácido Ascórbico/uso terapéutico , Ácido Ascórbico/administración & dosificación , Ácido Ascórbico/farmacología , Microbioma Gastrointestinal/efectos de los fármacos , Artritis Reumatoide/tratamiento farmacológico , Artritis Reumatoide/microbiología , Ratones , Artritis Experimental/tratamiento farmacológico , Artritis Experimental/microbiología , Artritis Experimental/inmunología , Masculino , Ratones Endogámicos DBA , Factor de Necrosis Tumoral alfa/metabolismo , Interleucina-6/metabolismo , Modelos Animales de Enfermedad , ARN Ribosómico 16S/genética
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