Abstract
Purpose The effect of Actovegin (R) was investigated on PMA- and LPS-induced human peripheral blood mononuclear cells (PBMCs). Methods PBMCs (1 x 10(6) cells/ml) from five blood donors (2 f, 3 m; 45-55 years) were grown in medium and exposed to Actovegin (R) in the presence or absence of PMA or LPS. Supernatants were collected to assess the concentration of cytokines (TNF-alpha, IL-1beta, IL-6 ...
Abstract
Purpose The effect of Actovegin (R) was investigated on PMA- and LPS-induced human peripheral blood mononuclear cells (PBMCs). Methods PBMCs (1 x 10(6) cells/ml) from five blood donors (2 f, 3 m; 45-55 years) were grown in medium and exposed to Actovegin (R) in the presence or absence of PMA or LPS. Supernatants were collected to assess the concentration of cytokines (TNF-alpha, IL-1beta, IL-6 and IL-10). The reactive oxygen species (ROS) were assessed by a ROS-Glo(TM) H2O2 assay. Results Stimulation of cells by PMA or LPS (without Actovegin (R)) significantly increased the secretion of IL-1beta, IL-6, IL-10 and TNF-alpha from PBMCs, compared to controls. Pre-treatment of cells with Actovegin (R) (1, 5, 25, 125 mu g/ml) plus PMA significantly decreased the secretion of IL-1beta from PBMCs, compared to controls (PMA without Actovegin (R)). In contrast, addition of Actovegin (R) (1, 5, 25, 125 and 250 mu g/ml) plus LPS did not alter the IL-1beta production, compared to controls (LPS without Actovegin (R)). TNF-alpha, IL-6 and IL-10 do not contribute to the reduction of inflammatory reactions with Actovegin (R). Conclusions Actovegin (R) can reduce the PMA-induced IL-1beta release and the ROS production from PBMCs. These findings may help to explain the clinically known positive effects of Actovegin (R) on athletic injuries with inflammatory responses (e.g., muscle injuries, tendinopathies).
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