Brazilin blocks catabolic processes in human osteoarthritic chondrocytes via inhibition of NFKB1/p50.
J Orthop Res
; 36(9): 2431-2438, 2018 09.
Article
em En
| MEDLINE
| ID: mdl-29704279
ABSTRACT
This study aimed to evaluate the chondroprotective and anti-inflammatory activity of brazilin in human osteoarthritic (OA) cartilage and chondrocytes with particular focus on the nuclear factor-kappa B (NF-κB) pathway. Therefore, brazilin was isolated from Caesalpinia sappan and identified using high performance liquid chromatography (HPLC). The effect of brazilin was assessed in cartilage explants treated with 10 ng/ml interleukin (IL)-1ß and 10 ng/ml tumor necrosis factor (TNF)-α using histological and biochemical glycosaminoglycan (GAG) analyses and in primary chondrocytes treated with 10 ng/ml IL-1ß using RT-qPCR, ELISA, and Western blot. The involvement of NF-κB signaling was examined using a human NF-κB signaling array and in silico pathway analysis. Brazilin was found to reduce the GAG loss from cartilage explants stimulated with IL-1ß and TNF-α. NF-κB pathway analysis in chondrocytes revealed NFKB1/p50 as a central player regulating the anti-inflammatory activities of brazilin. Brazilin suppressed the IL-1ß-mediated up-regulation of OA markers and the induction of NFKB1/p50 in chondrocytes. In conclusion, brazilin effectively attenuates catabolic processes in human OA cartilage and chondrocytes-at least in part due to the inhibition of NFKB1/p50-which indicates a chondroprotective potential of brazilin in OA. © 2018 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 362431-2438, 2018.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Osteoartrite
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Benzopiranos
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Cartilagem Articular
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Condrócitos
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Subunidade p50 de NF-kappa B
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Anti-Inflamatórios
Tipo de estudo:
Prognostic_studies
Limite:
Aged
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Aged80
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Female
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Humans
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Male
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Middle aged
País/Região como assunto:
America do sul
/
Brasil
Idioma:
En
Revista:
J Orthop Res
Ano de publicação:
2018
Tipo de documento:
Article
País de afiliação:
Áustria