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Chelidonine reduces IL-1β-induced inflammation and matrix catabolism in chondrocytes and attenuates cartilage degeneration and synovial inflammation in rats

Authors :
Mao Li
Ying Zhu
Jiajia Shao
Chuanbing Wang
Bin Dong
Haiyong Cui
Dongdong Dai
Source :
Brazilian Journal of Medical and Biological Research, Vol 56 (2023)
Publication Year :
2023
Publisher :
Associação Brasileira de Divulgação Científica, 2023.

Abstract

Chondrocyte inflammation and catabolism are two major features in the progression of osteoarthritis (OA). Chelidonine, a principal alkaloid extracted from Chelidonium majus, is suggested to show anti-inflammation, anti-apoptosis, and anti-oxidation activities in various diseases. However, its potential effects on OA cartilage degeneration remains unclear. To evaluate the effect of chelidonine on OA and its underlying mechanism, we incubated chondrocytes with interleukin (IL)-1β and chelidonine at varying concentrations. Then, we performed the CCK-8 assay, fluorescence immunostaining, reverse transcription PCR, ELISA, and western blotting to evaluate cell viability, catabolic/inflammatory factors, levels of extracellular matrix (ECM)-related proteins, and the involved pathways. H&E and Safranin-O staining and ELISA were performed to measure cartilage degradation and synovial inflammation. Chelidonine suppressed the IL-1β-mediated catabolism and inflammation of chondrocytes. Chelidonine suppressed the NF-κB pathway activation. Similarly, our in vivo experiment showed that chelidonine partially attenuated cartilage degradation while inhibiting synovial inflammation. Chelidonine inhibited inflammation and catabolism through modulation of NF-κB pathways in vitro, thereby avoiding rat cartilage degeneration and synovial inflammation within OA.

Details

Language :
English
ISSN :
1414431X and 1414431x
Volume :
56
Database :
Directory of Open Access Journals
Journal :
Brazilian Journal of Medical and Biological Research
Publication Type :
Academic Journal
Accession number :
edsdoj.f3c64facfa3478a944e7b184494c407
Document Type :
article
Full Text :
https://doi.org/10.1590/1414-431x2023e12604