New Approaches in the Regulation of Blood Phagocytes and Reduction in the Formation of Oxygen Radicals in Patients with Heart Failure

Abstract

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 (O 2 -•) 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 dosadependent 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 various organs and tissues, including blood cells and neurons that die as a result of ischemia and inflammation ВведениеНарушение сократительной активности сердца -синдром сердечной недостаточности (СН) -лежит в основе системной ишемии различных органов и тка-ней, включая сердце. Следствием является не только изменение функциональной активности этих органов, но и повреждение высокоэнергозависимых кле-