PubMed Health⌕ Search

Biomedical subjects

V I Kulikov

Publications and source records attributed to V I Kulikov.

At least 19 recordsLinked to original sources
PubMed2001

Inhibition of human platelet aggregation by amides and ester of salicylic acid with platelet-activating factor analogs.

The influence of acetyl salicylic acid (ASA) derivatives with platelet-activating factor (PAF) lipid analogs on PAF-induced human platelet aggregation has been studied. It was found that the ASA amide with an ethanolamine plasmalogen PAF analog (1-0-alk-1'-enyl-2-acetyl-sn-glycero-3-phospho-(N-2'-acetoxybenzoyl)ethanolamine) and the ASA ester with a choline plasmalogen PAF analog (1-0-alk-1'-enyl-2-(2'-acetoxybenzoyl)-sn-glycero-3-phosphocholine) at concentrations of 10-7-10-6 M effectively inhibit PAF-induced aggregation of human platelets. In contrast to these compounds, the ASA amide with an alkyl PAF analog (1-0-alkyl-2-acetyl-sn-glycero-3-phospho-(N-2'-acetoxybenzoyl)ethanolamine) did not inhibit PAF-induced platelet aggregation. As possible mechanisms of action of the studied compounds, the blockade of PAF-receptor and cyclooxygenase inhibition are proposed.

Amides↗
PubMed2000

Bioactive amide of prostaglandin E1 and ethanolamine plasmalogen analog of platelet-activating factor inhibits several pathways of human platelet aggregation.

The influence of an amide of prostaglandin E1 and ethanolamine plasmalogen platelet-activating factor analog 1-O-alk-1;-enyl-2-acetyl-sn-glycero-3-phospho-(N-11alpha, 15alpha-dioxy-9-keto-13-prostenoyl)ethanolamine (PGE1-PPAF) on platelet-activating factor (PAF)-, ADP-, and thrombin-induced human platelet aggregation has been studied. It was found that PGE1-PPAF inhibits the PAF-, ADP-, and thrombin-induced platelet aggregation in platelet-rich plasma. 1-O-alk-1;-enyl-2-acetyl-sn-glycero-3-phosphoethanolamine inhibited PAF-induced aggregation up to 50% but had no influence on platelet aggregation induced by ADP or thrombin. The ethanolamine plasmalogen analog of PAF 1-O-alk-1;-enyl-2-acetyl-sn-glycero-3-phospho-(N-palmitoyl)ethanolami ne, having a palmitoyl residue instead of PGE1, did not inhibit platelet aggregation induced by PAF, ADP, or thrombin. We propose that inhibition of human platelet aggregation by PGE1-PPAF is mediated by its action on platelet PAF-receptors and the adenylate cyclase system.

Alprostadil↗
PubMed1999

[Lipoprotein oxidation in the blood of women with pregnancy complications].

The level of lipoprotein oxidation in blood sera of pregnant women with obstetrical abnormalities is studied. Lipid peroxides were measured by a modified thiobarbituric acid test. The level of lipoprotein oxidation was increased, which may be one of the pathogenetic mechanisms of vascular disease in fetoplacental insufficiency and gestosis.

Adult↗
PubMed1999

Mechanisms of interaction of a plasmalogenic analog of platelet-activating factor with human platelets.

The interaction of a plasmalogenic analog of platelet-activating factor (1-O-alk-1;-enyl-2-acetyl-sn-glycero-3-phosphocholine; 1-alkenyl-PAF) with human platelets was studied. 1-Alkenyl-PAF induced an increase in intracellular Ca2+ concentration and inhibition of adenylate cyclase at significantly higher concentrations than PAF. 1-Alkenyl-PAF inhibits PAF-induced platelet aggregation but has no effect on ADP- or thrombin-induced aggregation of human platelets. In contrast to PAF, 1-alkenyl-PAF increases [3H]PGE1 binding with human platelets. The properties of 1-alkenyl-PAF as an agonist or antagonist of PAF receptors apparently depend on its concentration in the cell medium. Under physiological conditions 1-alkenyl-PAF might be a natural PAF antagonist acting in the human cardiovascular system.

Adenylyl Cyclase Inhibitors↗
PubMed1998

The bioregulatory role of platelet-activating factor in intracellular processes and cell-cell interactions.

The role of platelet-activating factor (PAF, a phospholipid compound) in regulation of cell functions and cell-cell interactions is reviewed. The biological effects of PAF on platelets, neutrophils, basophils, eosinophiles, lymphocytes, and endothelial cells are described. Mechanisms of cell activation by PAF are discussed. Interactions of PAF with other biological regulators (prostaglandins, leukotrienes, NO, tumor necrosis factor, and interleukins) are considered.

Animals↗
PubMed1997

[Immunoenzyme analysis in the determination of antibodies to main classes of cell phospholipids in human blood].

A modified ELISA is proposed for detecting antiphospholipid antibodies of the IgM and IgG isotypes, including antibodies to cardiolipin, phosphatidylserine, phosphatidylethanolamine, phosphatidylinositol, phosphatidylcholine, and sphingomyelin in human blood serum. The degree of phospholipid saturation, its phase (lamellar or hexagonal), purity, oxidation index of the phospholipid preparation, and conditions of solid phase treatment are important factors providing a sufficiently high sensitivity and reliability of measurements. The clinical value of the method was demonstrated in examinations of 70 patients with habitual abortions. The method can be used in studies of the spectrum of antiphospholipid antibodies in different diseases involving an increase of their blood serum level.

Adult↗
PubMed1997

Ether lipids and platelet-activating factor: evolution and cellular function.

This review considers the relation between the evolution of ether lipids and platelet-activating factor (PAF) in living organisms for the first time. Ether lipids are shown to be the main structural lipid components in the cells of the most primitive organisms on the Earth; during evolution they were gradually substituted for lipids with ester and vinyl bonds. Synthesis of PAF has been found in some bacteria, protozoans, yeasts, plants, marine invertebrates, lower vertebrates, and mammals. The regulatory role of PAF is suggested to already appear in protozoans and later be maintained during the subsequent evolution of living organisms. During evolution, functions of PAF in the cell have been changing and enlarging, while ether lipids have been gradually losing their role as the main structural lipid component of the cells of living organisms.

Animals↗
PubMed1996

[Biological role of cellular metabolites--structural analogs of platelet activating factor].

The review is concerned with cell metabolites - the platelet activating factor (PAF) and its choline-containing structural analogs. The biological activity of PAF and its analogs are considered. The influence of PAF and its analogs of membrane properties, cell receptors, transmembrane signalling (protein kinase C activation, Ca2+ release) as well as its participation in cell phospholipases A2, C and D activation are considered. The intracellular function of PAF and its analogs is discussed in terms of their influence on prostaglandin and leukotriene biosynthesis as well as with reference to the biological activity of 1-acyl-2-acetyl-sn-glycerols and lysophosphatidylcholine. The function of cell-released PAF and its analogs is considered in connection with their influence on plasma lipoproteins, inter-cell PAF synthesis and different mechanisms of PAF and PAF analog-induced cell activation including cell priming, cell desensitization and receptor-dependent effects. It is concluded that PAF is an intracellular and intercellular mediator, whereas 1-acyl-PAF is an intracellular lipid bioregulator.

Animals↗
PubMed1996

[Effect of sn-2-acetylated analogs of phosphatidalic acid on release and aggregation of human platelets].

The influence of sn-2-acetylated analogs of phosphatidalic acid on the release reaction and aggregation of human platelets has been studied. It was found that phosphate-, phosphorylethanolamine- or phosphorylcholine-containing sn-2-acetylated analogs of phosphatidalic acid do not stimulate human platelet aggregation but inhibit the platelet-activating factor (PAF) induced platelet aggregation. The phosphatidalic acid analog, I-O-alk-1'-enyl-2-acetyl-sn-glycero-3-phosphate, stimulates human platelet release reaction measured by acridine orange release from human platelets in the same extent as does PAF. Other phosphatidalic acid analogs (1-O-alk-1'-enyl-2-acetyl-sn-glycero-3-phosphoethanolamine, 1-O-alk-1'-enyl-2-acetyl-sn-glycero-3-phosphocholine) inhibit acridine orange exocytosis from PAF-stimulated human platelets. It is concluded that the activity of sn-2-acetylated phosphatidalic acid analogs towards human platelets differs from those of corresponding ester and ether phosphatidalic acid analogs and, consequently, they may have another functional significance in the processes of platelet activation.

Acetylation↗
PubMed1994

[Interaction of 1-O-alkyl-2-methoxy-sn-glycero-3-phosphocholine and platelet activating factor with blood and tumor cells].

The effects of the platelet-activating factor (PAF) and the methoxy-PAF analog, 1-O-alkyl-2-methoxy-sn-glycero-3-phosphocholine, on platelet activation, oxidative burst in neutrophils and proliferation of K-562 and P815 cells have been studied. It has been found that the biological activity of methoxy-PAF for human platelets and neutrophils is commensurate with that of PAF. However, the cytotoxic properties of methoxy-PAF are much stronger than the cytotoxicity of PAF for tumour cells. It is concluded that the biological activity of methoxy-PAF is, to a great extent, due to its close structural resemblance to PAF as well as to the inability of cells to perform rapid metabolism of methoxy-PAF.

Animals↗
PubMed1992

[The effect of aldehydogenic and acyl structural analogs of platelet activating factor on the formation of superoxide radicals by human blood leukocytes].

The effects of plasmalogenic and acyl structural analogs of the platelet activation factor (PAF) on the superoxide radical production by human blood leukocytes were studied. It was found that 1-O-acyl-2-acetyl-sn-glycero-3-phosphocholine and 1-O-(1'-alkenyl)-2-acetyl-sn-glycero-3-phosphocholine stimulates the production of leukocyte superoxide radicals, their activity being comparable with that of PAF. Stimulation of superoxide radical production strongly depends on the structure of the polar heads of PAF analogs. It is supposed that choline-containing plasmalogenic and acyl PAF analogs may act as specific lipid mediators of the neutrophil function.

Acylation↗
PubMed1992

[Acyl and plasmalogen analogs of platelet activating factor--new lipid cellular bioregulators].

Recent data concerning two structural platelet-activating factor (PAF) analogs-1-O-acyl-2-acetyl-sn-glycero-3-phosphocholine (acyl-PAF) and 1-O-alk-1'-enyl-2-acetyl-sn-glycero-3-phosphocholine (vinyl-PAF) identified in some cells and tissues are reviewed. Isolation, identification, biosynthesis, and metabolism of acyl-PAF and vinyl-PAF are considered. The activity of acyl-PAF and vinyl-PAF towards platelets, leukocytes, isolated myocardium, and ileum as well as its in vivo activity are discussed. The influence of acyl-PAF and vinyl-PAF on PAF platelet interaction, Ca2+ mobilization, and platelet adenylate cyclase activity is considered. It is concluded that similar to PAF, acyl-PAF and vinyl-PAF should be regarded as a family of PAF lipid bioregulators.

Acylation↗
PubMed1991

[Effects of phospholipid platelet activation factor on proliferation of B-lymphocytes of the peripheral blood of healthy donors and patients with bronchial asthma].

The influence of the phospholipid platelet activation factor (PAF) was studied on pokeweed mitogen (PWM)-stimulated proliferation of peripheral blood lymphocytes in patients with bronchial asthma and normal subjects. It was found that PAF exerts dose-dependent activation with following suppression mainly on B-cells after its action on the whole population of lymphocytes activated by PWM. Besides, the influence of PAF on lymphocyte proliferation seemed to be mediated by monocytes since removal of monocytes from the whole population of mononuclear cells abolished the lymphocyte activation induced by PWM. Indomethacin inhibits lymphocyte proliferation activation induced by PAF. The results indicate that PAF has an effect on the IgE and IgG synthesis by blood B-lymphocytes in patients with bronchial asthma.

Adult↗
PubMed1991

[Interaction of cells from murine organs with liposomes of various composition].

The distribution of liposomes prepared from total mouse liver lipids and containing (3H)-labelled platelet activation factor in mouse organs was studied. It was shown that the majority of intraperitoneally injected liposomes prepared from total mouse liver lipids were transported to mouse liver and spleen. The interaction of liposomes with spleen cells in vitro revealed that the affinity of liposomes prepared from total spleen macrophage or total spleen lymphocyte lipids for mouse spleen cells was much higher than that of liposomes prepared from a model lipid mixture. The liposome binding to isolated spleen macrophages or lymphocytes was much higher than the liposome uptake by these cells in the total population of mouse spleen cells.

Animals↗
PubMed1990

[Liposomal polycarboxylic chelating agents for elimination of toxic metals from the body].

Experimental evidence is overviewed to show the efficacy of liposomal polycarboxylic acids in detoxication and elimination of radionuclides and toxic metals from animal organisms. It is shown that liposomal salt of ethylene diaminetetraacetic acid is retained by the organism for a longer time. The reported evidence indicates considerable advantages of liposomal diethylene triaminepentaacetic acid in elimination of mercury, cadmium, lead, gold, ytterbium, and plutonium from animal organisms (as compared to free acid forms). The liposomal diethylene triaminepentaacetic acid significantly reduced the general and specific cadmium toxicity of animals loaded with lethal doses of cadmium chloride. N,N'-bis-[2-hydroxybenzene]-ethylenediamine-N,N'-diacetic acid in the liposomal form considerably increased the iron elimination rate as compared to the chelating solution. A possibility is proposed on the use of diethylene triaminepentaacetic acid in the liposomal form for radionuclide and toxic metal elimination and carriage detection.

Acetates↗