Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10768593 | Biochemical and Biophysical Research Communications | 2005 | 5 Pages |
Abstract
In order to investigate if β-endorphins anti-inflammatory effect in cartilage-damaging states is mediated via tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β), we examined its influence on these two cytokines in vitro. Human articular chondrocytes were obtained from patients undergoing total knee arthroplasty and stimulated with β-endorphin (60-6000 ng/ml). Protein levels of TNF-α and IL-1β were measured by ELISA in supernatants from articular chondrocyte cultures. β-Endorphin significantly increased the levels of IL-1β for all concentrations used after 15 min incubation, and when stimulated with 600 and 6000 ng/ml after 24 h incubation. The opioid-induced increase in IL-1β was blocked by naltrexone in the group tested. TNF-α expression was also significantly stimulated by 60 and 600 ng/ml β-endorphin after 15 min, an effect blocked by naltrexone in the group tested. These findings indicate that the mechanism of β-endorphins anti-inflammatory influence in cartilage-damaging states is not apparently mediated via these two cytokines modulation.
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Authors
Nenad Andjelkov, Jan Elvenes, James Martin, Oddmund Johansen,