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Dygai A.M.,Russian Academy of Medical Sciences | Artamonov A.V.,Scientific Features Management Company | Bekarev A.A.,Russian Academy of Medical Sciences | Vereschagin E.I.,Russian Academy of Medical Sciences | And 9 more authors.
Bulletin of Experimental Biology and Medicine | Year: 2010

We studied the effect of immobilized hyaluronidase on hemopoiesis underconditions of cyclophosphamide- induced suppression. The preparation was shown to possess high hemostimulating activity. The stimulatory effect of hyaluronidase on the erithron was more pronounced than its effect on the granulocytic hemopoietic stem due to increase in functional activity of hemopoietic precursors and hemopoiesis-inducing microenvironment. © 2010 Springer Science+Business Media, Inc. Source


Dygai A.M.,Russian Academy of Medical Sciences | Zhdanov V.V.,Russian Academy of Medical Sciences | Zyuz'Kov G.N.,Russian Academy of Medical Sciences | Udut E.V.,Russian Academy of Medical Sciences | And 10 more authors.
Bulletin of Experimental Biology and Medicine | Year: 2011

We evaluated whether immobilized hyaluronidase can modify the hematotropic effect of immobilized granulocyte CSF (G-CSF). The preparation of immobilized hyaluronidase (50 arb. units per mouse) potentiated the specific effect of immobilized G-CSF on granulomonocytopoiesis. The preparation was shown to facilitate the indirect effect of immobilized G-CSF on hemopoiesis (stimulation of the erythroid and lymphoid hemopoietic stems). These changes were accompanied by an increase in functional activity of hemopoietic precursor cells, secretion of humoral factors by bone marrow myelokaryocytes, and concentration of hemopoietins in the serum. © 2011 Springer Science+Business Media, Inc. Source


Dygai A.M.,Russian Academy of Medical Sciences | Zhdanov V.V.,Russian Academy of Medical Sciences | Zyuz'kov G.N.,Russian Academy of Medical Sciences | Stavrova L.A.,Russian Academy of Medical Sciences | And 11 more authors.
Bulletin of Experimental Biology and Medicine | Year: 2011

The effect of immobilized granulocyte CSF on morphological characteristics and functional state of the liver was studied during chronic toxic hepatitis. The mechanisms of the therapeutic action of this agent were evaluated. The product had a strong hepatoprotective effect and exhibited the antiinflammatory and antisclerotic properties. The mechanism of activation of reserve systems for cell renewal (involved in restoration of the liver tissue) is probably related to an increase in proliferative activity of early precursor cells in the bone marrow, mobilization of these cells into the peripheral circulation, and directed homing into the liver tissue where they activate local regenerative mechanisms and prevent hepatocyte destruction. It should be emphasized that the concentration of SDF-1 increases in the liver tissue, but decreases in the bone marrow. These changes create the concentration gradient, which determines the migration of undifferentiated precursor cells to the liver. © 2011 Springer Science+Business Media, Inc. Source


Dygai A.M.,Russian Academy of Medical Sciences | Zyuzkov G.N.,Russian Academy of Medical Sciences | Zhdanov V.V.,Russian Academy of Medical Sciences | Udut E.V.,Russian Academy of Medical Sciences | And 12 more authors.
Bulletin of Experimental Biology and Medicine | Year: 2011

Immobilized hyaluronidase (nanotechnology method of electron-beam synthesis) exhibited high hepatoprotective activity on the model of Cl4-induced hepatitis. This agent produced anticholestatic, anti-inflammatory, and antisclerotic effects. These effects were shown to accompany stimulation of multipotent bone marrow precursors, mobilization of these cells into the peripheral blood, and cell migration to the target organ increasing the number of parenchymal progenitor cells in the liver. The mechanisms for targeted migration of progenitor cells suggest a decrease in SDF-1 production by bone marrow stromal cells and increase in the synthesis of this factor by microenvironmental cells of the liver tissue. © 2011 Springer Science+Business Media, Inc. Source

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