Publications by authors named "N E Volskiĭ"

Aim: Evaluate the effect of experimental hyperlipidemia on the intensity of development of acute graft-versus-host reaction (GVHR) in mice.

Materials And Methods: Half-allogenic system C57Bl/6 (C57Bl/6 x DBA/2)F1 was used as a laboratory model of acute GVHR. Experimental hyperlipidemia in mice-recipients was induced by repeated administration of poloxamer 407.

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[Laboratory model of hyperlipidemia].

Zh Mikrobiol Epidemiol Immunobiol

October 2010

Aim: Approbation of laboratory model of hyperlipidemia induced by multiple administration of poloxamer 407 to hybrid mice (C57BL/6 x DBA/2) F1.

Materials And Methods: Two-month-old female mice (C57B1/6 x DBA/2)F1 were used for experiments. Level of dyslipidemia was assessed measuring cholesterol level in serum by method with cholesteroloxidase.

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The influence of tumor necrosis factor a (TNF-alpha) and media, conditioned by activated macrophages and lymphocytes and containing a complex of biologically active compounds (including cytokines), on the parameters of lipid metabolism in macrophages was studied. The addition of recombinant TNF-alpha and immunocompetent cell-conditioned media to mouse peritoneal macrophages culture stimulated labelled oleate incorporation into cholesterol esters and triglycerides, as well as labelled glycerine incorporation into cholesterol esters, but inhibited labelled cholesterol incorporation into cholesterol esters. One of the mechanisms of the influence of activated immunocompetent cells on cholesterol metabolism in macrophages was, supposedly, the stimulation of sphigmomyelinase activity by a complex of anti-inflammatory cytokines produced by these cells on their activation.

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Intravenous injection of acetylated low density lipoproteins (acLDL) in mice in a dose of 0.5 mg per mouse decreased the intensity of humoral immune response to sheep red blood cells (SRBC) by 35%. The addition of acLDL to mouse peritoneal macrophages in vitro resulted in inhibition of Fc-dependent phagocytosis of SRBC and fourfold increased secretion of prostaglandins E2 by macrophages.

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