Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 1 de 1
Filtrar
Mais filtros

Base de dados
Ano de publicação
Tipo de documento
Intervalo de ano de publicação
1.
Pharm Biol ; 61(1): 1431-1445, 2023 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-37674371

RESUMO

CONTEXT: Duhuo Jisheng pill (DHJS) is a classic traditional Chinese medicine (TCM) formula for rheumatoid arthritis (RA). The effective components and therapeutic mechanisms of DHJS for treating RA are still unclear. OBJECTIVE: To explore the potential mechanism of DHJS against RA by means of network pharmacology and experimental verification. MATERIALS AND METHODS: A network pharmacology and molecular docking analysis based on phytochemistry was used to elucidate the mechanism of DHJS against RA. The targets of DHJS anti-RA active ingredient were obtained by searching TCMSP, ETCM and TCMSID. The RA model induced by collagen was established in Wistar rats. The rats in the DHJS group were administered doses of 0.5, 1.0 and 2.0 g/kg for a period of 10 d. The expression of targets was measured with Western blot. RESULTS: Network pharmacology analysis showed that the anti-RA effect of DHJS was mediated by targets involved in immunity, inflammation and apoptosis, as well as PI3K-Akt and NF-κB signalling pathways. Of 2.0 g/kg DHJS significantly alleviated the ankle inflammation (IL-6: 62.73 ± 8.39 pg/mL, IL-1ß: 50.49 ± 11.47 pg/mL, TNF-α: 16.88 ± 3.05 pg/mL, IL-17A: 12.55 ± 1.87 pg/mL, IL-10: 16.24 ± 3.00 pg/mL), comparing with the model group (IL-6: 92.02 ± 13.25 pg/mL, IL-1ß: 71.85 ± 4.12 pg/mL, TNF-α: 25.64 ± 3.69 pg/mL, IL-17A: 22.14 ± 4.56 pg/mL, IL-10: 9.51 ± 3.03 pg/mL) (p < 0.05). Moreover, the protein expression of p-PI3K, p-AKT and p-p65 significantly decreased after DHJS administration. CONCLUSIONS: DHJS could alleviate the collagen-induced arthritis (CIA) by the PI3K/AKT/NF-κB signalling pathway.


Assuntos
Artrite Reumatoide , NF-kappa B , Animais , Ratos , Ratos Wistar , Simulação de Acoplamento Molecular , Interleucina-10 , Interleucina-17 , Interleucina-6 , Farmacologia em Rede , Fosfatidilinositol 3-Quinases , Proteínas Proto-Oncogênicas c-akt , Fator de Necrose Tumoral alfa , Artrite Reumatoide/tratamento farmacológico , Inflamação
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA