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Icariin represses the inflammatory responses and survival of rheumatoid arthritis fibroblast-like synoviocytes by regulating the TRIB1/TLR2/NF-kB pathway.
Wu, Zhi-Ming; Xiang, Yan-Ru; Zhu, Xiao-Bo; Shi, Xiao-Dong; Chen, Sha; Wan, Xin; Guo, Jian.
Afiliación
  • Wu ZM; Department of Traditional Chinese Medicine, The First Affiliated Hospital of Nanchang University, Nanchang 330000, Jiangxi Province, PR China.
  • Xiang YR; Department of Traditional Chinese Medicine, The First Affiliated Hospital of Nanchang University, Nanchang 330000, Jiangxi Province, PR China.
  • Zhu XB; Department of Traditional Chinese Medicine, The First Affiliated Hospital of Nanchang University, Nanchang 330000, Jiangxi Province, PR China.
  • Shi XD; Department of Rheumatology, The Affiliated Hospital of Jiangxi University of Traditional Chinese Medicine, Nanchang 330000, Jiangxi Province, PR China.
  • Chen S; Department of Traditional Chinese Medicine, The First Affiliated Hospital of Nanchang University, Nanchang 330000, Jiangxi Province, PR China.
  • Wan X; Department of Traditional Chinese Medicine, The First Affiliated Hospital of Nanchang University, Nanchang 330000, Jiangxi Province, PR China.
  • Guo J; Department of Traditional Chinese Medicine, The First Affiliated Hospital of Nanchang University, Nanchang 330000, Jiangxi Province, PR China. Electronic address: aguojian761@163.com.
Int Immunopharmacol ; 110: 108991, 2022 Sep.
Article en En | MEDLINE | ID: mdl-35792272
BACKGROUND: Effective treatment methods for rheumatoid arthritis (RA) are still lacking. Previous studies have shown that icariin exerts a significant therapeutic effect on RA; however, the molecular mechanism requires further analysis. METHODS: qRT-PCR and western blot were performed to examine the gene or protein levels, respecctively. The proinflammatory cytokine levels were determined utilizing ELISA and western blot assays. Cell proliferation and apoptosis were quantified using CCK-8, EdU and flow cytometry assays, respectively. A RA mouse model was established to observe histopathological changes. RESULTS: Both icariin treatment and TRIB1 overexpression inhibited proliferation and inflammatory responses but promoted the apoptosis of TNF-α-treated RA-FLSs. Icariin treatment increased TRIB1 expression by promoting Nrf2 expression, thus blocking TLR2/NF-κB signalling. In addition, functional rescue experiments suggested that TRIB1 knockdown strikingly restrained the biological effects of icariin on TNF-α-treated RA-FLSs. Moreover, in vivo experimental results revealed that icariin restored inflammation and deterioration in RA mice by upregulating TRIB1. CONCLUSIONS: Based on these results, icariin repressed TNF-α-induced inflammatory responses and survival in RA-FLSs by regulating the TRIB1/TLR2/NF-kB pathway, implying that icariin may be a promising candidate drug for RA treatment.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Artritis Reumatoide / Sinoviocitos Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: Int Immunopharmacol Asunto de la revista: ALERGIA E IMUNOLOGIA / FARMACOLOGIA Año: 2022 Tipo del documento: Article Pais de publicación: Países Bajos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Artritis Reumatoide / Sinoviocitos Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: Int Immunopharmacol Asunto de la revista: ALERGIA E IMUNOLOGIA / FARMACOLOGIA Año: 2022 Tipo del documento: Article Pais de publicación: Países Bajos