Abstract
Emodin, an anthraquinone isolated from the Chinese herb Radix et Rhizoma Rhei, has been reported to have anti-inflammatory, antibacterial, and antitumor activities. However, the effect of emodin on collagen-induced arthritis (CIA) has not yet been investigated. The purpose of this study was to investigate whether emodin has a protective effect against collagen-induced arthritis in mice and its possible mechanisms. CIA was induced in mice by immunization with bovine type II collagen. The mice were treated with emodin (5, 10, and 20 mg/kg/day, i.g.) from days 21 to 42 after immunization. The clinical scores and hind paw swelling were evaluated. The expression of prostaglandin E2 (PGE2) and cyclooxygenase-2 (COX-2) in synovial tissues was determined. The levels of tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6) in the plasma were measured by enzyme-linked immunosorbent assay. The results showed that emodin treatment significantly alleviated the severity of the disease, based on the reduced hind paw swelling and clinical scores, compared with untreated CIA mice. Comparing with untreated CIA mice, emodin treatment inhibited the levels of TNF-α and IL-6 in the plasma, PGE2 production, and COX-2 protein expression in synovial tissues in a dose manner. In conclusion, our results suggest that anti-inflammatory effects of emodin against collagen-induced arthritis in mice may be due to its ability to inhibit pro-inflammatory mediators. Emodin may be a promising potential therapeutic reagent for arthritis treatment.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
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.