Effect of rutoside (RU) treatment on rat inflammatory mediators. (a) Sera were collected at day 50 after immunization and tested for their concentrations in tumor necrosis factor-alpha (TNF-α), prostaglandin E2 (PGE2), interleukin-1-beta (IL-1β), and monocyte chemoattractant protein-1 (MCP-1). Results are shown as mean percentage of modulation of cytokine levels compared to healthy rats. Mean percentage + standard deviation from three rats in each group is shown. P value compared to untreated adjuvant-induced arthritis (AIA) rats. (b) Freshly isolated peritoneal macrophages from untreated or RU-treated rats were collected on day 50 after immunization. They were incubated in medium alone during 48 hours, and their supernatants were collected and tested for their TNF-α or nitrite levels. P value compared to untreated AIA rat cells. (c) Macrophages from normal rats were incubated in medium alone or activated by lipopolysaccharide. RU was added (50 μM) simultaneously to cell activation. Cell supernatants were harvested 48 hours after incubation and tested for their concentrations of TNF-α, PGE2, IL-1β, and MCP-1. P value compared to activated cells. (d) RU inhibits the release of nitric oxide from activated rat macrophages in a dose-dependent manner. Bars show mean + standard deviation from three different rat cell preparations. P value compared to activated cells.
Kauss et al. Arthritis Research & Therapy 2008 10:R19 doi:10.1186/ar2372