In Vivo Study to Explore the Antiarthritic Potential of Tiliroside on Complete Freund’s Adjuvant-Induced Rheumatoid Arthritis in Rats
摘要
The purpose of this research was to examine the pharmacological properties and potential mechanism of action of tiliroside in rheumatoid arthritis. To mimic the effects of this autoimmune and inflammatory disease, male Sprague-Dawley rats were injected with complete Freund’s adjuvant (0.1 ml/rat) and then given tiliroside at doses of 5, 10, and 20 mg/kg. Tiliroside effectively decreases hind paw volume and its swelling ratio perimeter, leading to an increase in body weight in tested rats. It revealed a considerable reduction in the rheumatoid arthritis serum biomarkers, e.g., rheumatoid factor, C-reactive protein, and serum anti-cyclic citrullinated peptide (anti-CCP) antibodies. In addition to an increase in anti-inflammatory IL-4 and IL-10, tiliroside treatment was shown to dramatically reduce cytokines levels for tumor necrosis factor alpha (TNF-α), interleukins IL-1β and IL-6, monocyte chemoattractant protein-1 (MCP-1), the chemokine RANTES (regulated upon activation, normal T cell expressed, and secreted chemokine, also called CCL5), and interleukin-17 A. Matrix metalloproteinase 9 was inhibited by tiliroside, but MMP-2 was upregulated, in injected rats with complete Freund’s adjuvant. Modulation of malonaldehyde, superoxide dismutase, and glutathione levels in the tiliroside-treated group was also observed to lower oxidative stress. Inhibition of COX-2 by tiliroside in blood and joint tissues of rats treated with complete Freund’s adjuvant was dose-dependent, as shown by enzyme-linked immunosorbent assay and western blotting. The results indicate that tiliroside has promising antiarthritic properties and may be useful in the treatment of rheumatoid arthritis.
Graphical Abstract