Abstract
Background. We have previously reported a continuous activation of caspase-1 and increased interleukin (IL)-1β levels in early rheumatoid arthritis (RA). These observations raised the hypothesis that drugs targeting the IL-1β pathway, in addition to tumour necrosis factor (TNF), may be particularly effective for early RA treatment. We have recently identified gambogic acid as a promising therapeutic candidate to simultaneously block IL-1β and TNF secretion. Our main goal here was to investigate whether gambogic acid administration was able to attenuate inflammation in antigen-induced arthritis (AIA) rats. Methods. Gambogic acid was administered to AIA rats in the early and late phases of arthritis. The inflammatory score, ankle perimeter, and body weight were evaluated during the period of treatment. Rats were sacrificed after 19 days of disease progression and paw samples were collected for histological and immunohistochemical evaluation. Results. We found that inflammation in joints was significantly suppressed following gambogic acid administration. Histological and immunohistochemical evaluation of treated rats revealed normal joint structures with complete abrogation of the inflammatory infiltrate and cellular proliferation. Conclusions. Our results suggest that gambogic acid has significant anti-inflammatory properties and can possibly constitute a prototype anti-inflammatory drug with therapeutic efficacy in the treatment of inflammatory diseases such as RA.
Highlights
Rheumatoid arthritis (RA) is the most common disease of the inflammatory joint diseases, afflicting about 1% of the world population
Our results demonstrated that treatment with gambogic acid protected Wistar antigen-induced arthritis (AIA) rats from arthritis development with a complete abrogation of joint immune cellular infiltration and proliferation, preventing cartilage and bone damage
We have found that Wistar AIA rats can be effectively treated by gambogic acid
Summary
Rheumatoid arthritis (RA) is the most common disease of the inflammatory joint diseases, afflicting about 1% of the world population. We have previously reported increased levels of IL-1β in very recent onset arthritis and in the synovial fluid of established RA patients [5] This observation could be explained by the activation of caspase-1 that we have observed both in early and established RA patients [6]. We have previously reported a continuous activation of caspase-1 and increased interleukin (IL)-1β levels in early rheumatoid arthritis (RA). These observations raised the hypothesis that drugs targeting the IL-1β pathway, in addition to tumour necrosis factor (TNF), may be effective for early RA treatment.
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