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Curcumin inhibits pro-inflammatory mediators and metalloproteinase-3 production by chondrocytes

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Abstract

Objective and design

This study aims to investigate the effects of curcumin (Cur) on the extracellular matrix protein metabolism of articular chondrocytes and on their production of inflammatory mediators.

Methods

Human chondrocytes in alginate beads and human cartilage explants were cultured in the absence or in the presence of interleukin (IL)-1beta (10−11 M) and with or without Cur (5–20 μM). Nitric oxide (NO) synthesis was measured by the Griess spectrophotometric method; prostaglandin (PG) E2 by a specific radioimmunoassay; and IL-6, IL-8, aggrecan (Agg), matrix metalloproteinase (MMP)-3, and tissue inhibitor of metalloproteinase (TIMP)-1 by specific enzyme-amplified immunoassays. Proteoglycan degradation was evaluated by the release of 35S-glycosaminoglycans (GAG) from human cartilage explants.

Results

In alginate beads and cartilage explant models, Cur inhibited the basal and the IL-1beta-stimulated NO, PGE2, IL-6, IL-8, and MMP-3 production by human chondrocytes in a concentration-dependent manner. The TIMP-1 and the Agg productions were not modified. In the basal condition, 35S-GAG release from cartilage explants was decreased by Cur.

Conclusions

Curcumin was a potent inhibitor of the production of inflammatory and catabolic mediators by chondrocytes, suggesting that this natural compound could be efficient in the treatment of osteoarthritis.

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Acknowledgments

The work was supported by an educational grant from BioXtract. Christelle Sanchez is a Postdoctoral Researcher of the National Fund for Scientific Research (FNRS, Belgium). The authors extend their appreciation to Paul Simonis and Murielle Lemestre (Centre Hospitalier Universitaire de Liège) for their skillful technical assistance.

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Correspondence to Y. Henrotin.

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Responsible Editor: J. Di Battista.

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Mathy-Hartert, M., Jacquemond-Collet, I., Priem, F. et al. Curcumin inhibits pro-inflammatory mediators and metalloproteinase-3 production by chondrocytes. Inflamm. Res. 58, 899–908 (2009). https://doi.org/10.1007/s00011-009-0063-1

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  • DOI: https://doi.org/10.1007/s00011-009-0063-1

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