Ellagic acid alleviates adjuvant induced arthritis by modulation of pro- and anti-inflammatory cytokines

Rheumatoid arthritis (RA) is a chronic inflammatory disease of unknown aetiology, but it is now clear that pro-inflammatory cytokines play a central role in its pathogenesis. Ellagic acid (EA) has a variety of biological activities including anti-oxidant, anti-inflammatory, and anti-cancer properties. The aim of the present study was to evaluate the potential effect of ellagic acid on the prevention and/or treatment of adjuvant induced arthritis (AIA) model in mice. Ellagic acid treatment was started one week before AIA induction and continued for three weeks after induction of AIA. Ellagic acid treatment significantly (p 0.01) inhibited foot paw oedematous swelling and attenuated AIA-associated pathology. Ellagic acid significantly (p 0.01) reduced serum levels of pro-inflammatory cytokines: interleukin 1 (IL-1), tumor necrosis factor (TNF-), and interleukin 17 (IL-17). However, serum levels of IL-10 and interferon (IFN-) significantly increased (p 0.01 and p 0.05, respectively), while serum level of transforming growth factor (TGF-) did not significantly alter with EA treatment. In conclusion, these results suggest that EA attenuated AIA-associated pathology in the mouse model by downregulation of pro-inflammatory cytokines and upregulation of anti-inflammatory cytokines

Hesperidin Inhibits Inflammatory Response Induced by Aeromonas hydrophila Infection and Alters CD4+/CD8+ T Cell Ratio

Background. Aeromonas hydrophila is an opportunistic bacterial pathogen that is associated with a number of human diseases. Hesperidin (HES) has been reported to exert antioxidant and anti-inflammatory activities. Objectives. The aim of this study was to investigate the potential effect of HES treatment on inflammatory response induced by A. hydrophila infection in murine. Methods. A. hydrophila-infected mice were treated with HES at 250 mg/kg b.wt./week for 4 consecutive weeks. Phagocytosis, reactive oxygen species production, CD4+/CD8+ T cell ratio, and CD14 expression on intestinal infiltrating monocytes were evaluated. The expression of E-selectin and intercellular adhesion molecule 1 on stimulated HUVECs and RAW macrophage was evaluated. Results. Percentage of CD4+ T cells in the intestinal tissues of infected treated mice was highly significantly increased; however, phagocytic index, ROS production, CD8+ T cells percentage, and CD14 expression on monocytes were significantly reduced. On the other hand, HES significantly inhibited A-LPS- and A-ECP-induced E-selectin and ICAM-1 expression on HUVECs and ICAM-1 expression on RAW macrophage. Conclusion. Present data indicated that HES has a potential role in the suppression of inflammatory response induced by A. hydrophila toxins through downmodulation of ROS production and CD14 and adhesion molecules expression, as well as increase of CD4+/CD8+ cell ratio

Ellagic acid alleviates adjuvant induced arthritis by modulation of pro-and anti- inflammatory cytokines

Abstract rheumatoid arthritis (ra) is a chronic inflammatory disease of unknown aetiology, but it is now clear that pro-inflammatory cytokines play a central role in its pathogenesis. Ellagic acid (Ea) has a variety of biological activities including anti-oxidant, anti-inflammatory, and anti-cancer properties. The aim of the present study was to evaluate the potential effect of ellagic acid on the prevention and/ or treatment of adjuvant induced arthritis (aia) model in mice. Ellagic acid treatment was started one week before aia induction and continued for three weeks after induction of aia. Ellagic acid treatment significantly (p < 0.01) inhibited foot paw oedematous swelling and attenuated aia-associated pathology. Ellagic acid significantly (p < 0.01) reduced serum levels of pro-inflammatory cytokines: interleukin 1β (il-1β), tumor necrosis factor α (TnF-α), and interleukin 17 (il-17). however, serum levels of il-10 and interferon γ (iFn-γ) significantly increased (