Abstract

BackgroundGanghwaljetongyeum (GHJTY), a complex herbal decoction, is used to treat rheumatoid arthritis. However, the action mechanism of GHJTY is not still unclear on rheumatoid arthritis. In this study, we examined the beneficial effects and the action mechanisms of GHJTY on synoviocyte proliferation and inflammatory mediators.MethodsTo test the effect of GHJTY on synoviocyte proliferation, HIG-82 cells, rabbit knee synovial membrane cells, were treated with GHJTY under IL-1β. To evaluate the effects of GHJTY on proinflammatory mediators, we tested cytokine levels in RAW264.7 cells.ResultsProliferation of HIG-82 cells was significantly inhibited by GHJTY treatment. We found that GHJTY caused cytoskeleton damage to HIG-82 cells. In contrast, treatment of GHJTY did not show any cytotoxicity to other different origin cell lines, HeLa and RAW264.7 cells. GHJTY inhibited IL-1β-mediated NF-κB activation in HIG-82 cells and reduced the LPS-mediated production of proinflammatory cytokines, TNF-α, IL-12, and NO in RAW264.7 cells. In addition, the expression of cyclooxygenase in LPS-activated RAW264.7 cells was also decreased by GHJTY treatment.ConclusionsThese results suggest that GHJTY might effectively attenuate rheumatoid arthritis by inhibiting the production of proinflammatory mediators and the proliferation of synoviocytes.

Highlights

  • Ganghwaljetongyeum (GHJTY), a complex herbal decoction, is used to treat rheumatoid arthritis

  • GHJTY suppresses the proliferation of HIG-82 cells To assess the effect of GHJTY on synoviocyte proliferation, HIG-82 cells were exposed to IL-1β and GHJTY for 2 days

  • IL-1β caused proliferation of HIG-82 cells, which was inhibited by Celecoxib, a non-steroidal anti-inflammatory drug used for the treatment of rheumatoid arthritis

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Summary

Results

Proliferation of HIG-82 cells was significantly inhibited by GHJTY treatment. We found that GHJTY caused cytoskeleton damage to HIG-82 cells. Treatment of GHJTY did not show any cytotoxicity to other different origin cell lines, HeLa and RAW264.7 cells. GHJTY inhibited IL-1β-mediated NF-κB activation in HIG-82 cells and reduced the LPS-mediated production of proinflammatory cytokines, TNF-α, IL-12, and NO in RAW264.7 cells. The expression of cyclooxygenase in LPS-activated RAW264.7 cells was decreased by GHJTY treatment

Conclusions
Background
Methods
Results and discussion
Muller-Ladner U
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