Abstract

We have previously reported an increase in interleukin (IL)-1β levels and a continuous activation of caspase-1 in rheumatoid arthritis (RA) patients in the early phase of the disease. This result suggests that drugs targeting IL-1β regulatory pathways, in addition to tumor necrosis factor (TNF), may constitute promising therapeutic agents in early RA. We have recently used a THP-1 macrophage-like cell line to screen 2320 compounds for those which down-regulate IL-1β and TNF secretion. Gambogic acid, celastrol and pristimerin were three of the most promising therapeutic candidates identified in that study.

Highlights

  • We have previously reported an increase in interleukin (IL)-1b levels and a continuous activation of caspase-1 in rheumatoid arthritis (RA) patients in the early phase of the disease

  • Aim Our main goal here is to investigate whether administration of gambogic acid, celastrol or pristimerin is able to attenuate inflammation in a rat model of antigen-induced arthritis (AIA)

  • Drugs were administered to AIA rats (N=5-10 per group) in the early phase of arthritis, after 4 days of disease induction and for a period of 15 days

Read more

Summary

Introduction

We have previously reported an increase in interleukin (IL)-1b levels and a continuous activation of caspase-1 in rheumatoid arthritis (RA) patients in the early phase of the disease. This result suggests that drugs targeting IL-1b regulatory pathways, in addition to tumor necrosis factor (TNF), may constitute promising therapeutic agents in early RA. Celastrol and pristimerin were three of the most promising therapeutic candidates identified in that study. Aim Our main goal here is to investigate whether administration of gambogic acid, celastrol or pristimerin is able to attenuate inflammation in a rat model of antigen-induced arthritis (AIA)

Methods
Results
Conclusions
Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.