OBJECTIVE Our aim was to study the effect of calf blood gemodializat on apoptosis and intracellular signaling pathways of neuroblastoma cells SK-N-SH human. METHODS Apoptosis was recorded by fluorescent microscopy using Hoechst 33342. Necrosis cells was monitored by propidium iodide. The fluorescence of the cells was recorded on a fluorescence inverted microscope Keyence BZ8100 (Japan). Formation of reactive oxygen species (ROS) in the cells of SK-N-SH was determined using nitroblue tetrazolium by absorbance at 620 nm on a plate reader "Uniplan". RESULTS When adding hydrogen peroxide to the background of the calf blood gemodializat been decreasing apoptosis of these cells with 43 to 17% relative to apoptosis in the presence of a hydrogen peroxide. Under these conditions, the calf blood gemodializat significantly reduced ROS formation in human neuroblastoma cells SK-N-SH by the action of hydrogen peroxide. In these cells, we investigated the influence of calf blood gemodializat on apoptosis and intracellular signaling pathway involving mitogen-activated protein kinase (p38MAPK), extracellular regulatory kinase (ERK), phosphatidylinositol 3-kinase (PI-3K) and-Jun-N-terminal kinase (JNK) using their selective inhibitors. CONCLUSION It was shown that the mechanism of the protective effect of calf blood gemodializat against peroxide-induced apoptosis in SK-N-SH dominant role is played by p38 MAPK and PI-3K.

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.

Aim. To study the influence of biogenic stimulators Actovegine and Zifodine (deproteinized hemodrivates of calf blood) on reactive oxygen species formation by blood phagocytes in patients with chronic heart failure (CHF).Material and methods. Reactive oxygen species formation was registered by lucigenine-dependent chemiluminiscence on the luminomenter “Biotox-7” (Russia) in 20 patients with CHF of II-III functional classes by NYHA. The hemiluminiscences basal and stimulated by farbolic ether (RMA) were measured, as also inhibitory activity of Actovegine and Zifodine.Results. In CHF patients’ blood there was “spontaneous” secretion superoxide anion radicals, that is showing presence of preactivated phagocytes. In addition, a significant increase of oxygen radicals is shown as a response to RMA (1 mcM). Actovegine and Zifodine dose-dependently suppressed prominence of the response. While concomitantly applied Actovegine and Zifodine at the RMA background there was additive inhibitory effect found, which was not depended on consequence of additives.Conclusion. Actovegine and Zifodine decrease reactive oxygen species secretion by phagocytes, which are extracted from the blood of CHF patients. Addictiveness of such inhibitory effects of Actovegine and Zifodine shows absence of their identity by structure and of improper translation of this data into conclusions on effectiveness and safety, found in clinical practice while prescribing Actovegine and Zifodine.

Objective : Our aim was to study the effect of calf blood gemodializat  on apoptosis and intracellular signaling pathways of neuroblastoma cells SK-N-SH human. Methods : Apoptosis was recorded by fluorescent microscopy using Hoechst 33342. Necrosis cells was monitored by propidium iodide. The fluorescence of the cells was recorded on a fluorescence inverted microscope Keyence BZ8100 (Japan). Formation of reactive oxygen species (ROS) in the cells of SK-N-SH was determined using nitroblue tetrazolium by absorbance at 620 nm on a plate reader «Uniplan». Results : When adding hydrogen peroxide to the background of the calf blood gemodializat been decreasing apoptosis of these cells with 43 to 17% relative to apoptosis in the presence of a hydrogen peroxide. Under these conditions, the calf blood gemodializat  significantly reduced ROS formation in human neuroblastoma cells SK-N-SH by the action of hydrogen peroxide. In these cells, we investigated the influence of calf blood gemodializat  on apoptosis and intracellular signaling pathway involving mitogen-activated protein kinase (p38MAPK), extracellular regulatory kinase (ERK), phosphatidylinositol 3-kinase (PI-3K) and-Jun-N-terminal kinase (JNK) using their selective inhibitors. Conclusion : It was shown that the mechanism of the protective effect of calf blood gemodializat   against peroxide-induced apoptosis in SK-N-SH dominant role is played by p38 MAPK and PI-3K.

A comparative evaluation has been carried out between the effects of surgical CO2-laser (lambda = 10.6 mcm) and lasers previously unused in medicine: Yag-erbium (lambda = 2.94 mcm) and YAG-erbium-in-glass lasers on biological tissue. The cutting properties of the lasers, nature of their effect on tissue and the period of healing of laser injury were studied morphologically. Effects of radiation on the energetic, biosynthetic and proliferative processes in the liver tissue, as well as the activity of transamination enzymes have been investigated. It has been shown that laser radiation of lambda = 1.54 and lambda = 2.94 mcm can destroy biological tissue with minimum inflammatory reaction as compared to CO2-laser. It has been ascertained that better marked changes in bioenergetics, aminotransferase activity, RNA and DNA contents are observed under the influence of CO2 and YAG-erbium lasers. Exposure of liver to YAG-erbium-in-glass laser radiation produced minimum changes in cells of the tissue contiguous to the injury. Thus, under its influence the majority of the investigated indices either changed insignificantly or improved. This might account for a positive effect of this laser on the dynamics and quality of the injury healing. The experimental studies gave basis for creation of working models of laser devices (lambda = 1.54 mcm) which are undergoing successful clinical trials at present.