[New approaches in the regulation of blood phagocytes and reduction in the formation of oxygen radicals in patients with heart failure].

AIM The purpose was to study the effect of actovegin on the formation of reactive oxygen species by blood phagocytes of patients with heart failure and on SK-N-SH neuron necrosis. MATERIALS AND METHODS The generation of superoxide anion (O2-*) were recorded on whole blood samples (50-100 μl). Change lucigenin-dependent hemiluminescence determined on a hemi-luminometer "Biotoks-7". As a stimulator of the phagocyte. phorbol ester (PMA, 1 μm) was used. Necrosis of neurons induced by hydrogen peroxide was determined by fluorescence of propidium iodit. RESULTS Blood phagocytes of heart failure patients are initially pre-activated (primed). These cells spontaneous generated oxygen radicals. Actovegin dosa-dependent decreased radicals level and radical induced by PMA (1 μm). After PMA maximal inhibitory effect of actovegin observed in doses higher than 2-3 mg/ml. The impact of actovegin on the viability of human SK-N-SH neurons in the presence hydrogen peroxide (100 μm) was studied in vitro. Under these conditions hydrogen peroxide triggered radical-dependent neurons necrosis Actovegin dosa-dependent decreased of neuron death. CONCLUSION Actovegin inhibits spontaneous and induced formation of reactive oxygen species generated by blood phagocytes of patients with heart failure. Actovegin suppressed necrosis of human SK-N-SH neuroblastoma cells caused by hydrogen peroxide. It is assumed that actovegin protects_cells of arious organs and tissues, including blood cells and neurons that die as a result of ischemia and inflammation by reducing levels of react.ive-oxygenspecies.