[NEUROPROTECTIVE EFFECT OF AMINOGUANIDINE IN EXPERIMENTAL OBSTETRIC ANTIPHOSPHOLIPID SYNDROME].

The aim of the research was to investigate the effect of aminoguanidine on the content of autoantibodies in the serum, nitric oxide synthesis (NO), glial fibrillary acidic protein (GFAP) content and indicators of free radical oxidation in the cerebral hemispheres of BALB/c mice with antiphospholipid syndrome (APS) on the 18th day of pregnancy. An increase in the content of autoantibodies to brain proteins (120 kDa, 150 kDa, and >170 kDa) was detected in the serum of BALB/c mice with APS on the 18th day of pregnancy. An increase in the content of GFAP (total), GFAP (49-37 kDa), NO2¯, NO3¯ and prooxidant-antioxidant system imbalance in the cerebral hemispheres of pregnant mice with APS was established. With administration of aminoguanidine into the pregnant mice with APS, a decrease in the content of autoantibodies to brain proteins (120 kDa and 150 kDa) in serum was proved. With the introduction of aminoguanidine, a selective inhibitor of inducible NO synthase on the 18th day of pregnancy the increase in GFAP (49-37 kDa) in the cerebral hemispheres of APS mice was established, and the GFAP (total), NO2¯ and NO3¯ content did not change significantly, relative to the indicators of pregnant animals with APS. With introduction of aminoguanidine in cases of APS on the 18th day of pregnancy lesser manifestations of oxidative stress in the cerebral hemispheres, a decrease in the activity of lipid peroxidation processes, an increase in the activity and content of the antioxidant system components was evidenced. Thus, aminoguanidine has a neuroprotective effect in obstetric antiphospholipid syndrome in the BALB/c mice.

[PRODUCTION OF REACTIVE OXYGEN SPECIES AND DEVELOPMENT OF APOPTOSIS IN BLOOD LEUKOCYTES IN EXPERIMENTAL ANTIPHOSPHOLIPID SYNDROME].

The aim of the study is to investigate the processes of apoptosis and the level of formation of reactive oxygen species (ROS) in blood cells of BALB/c female mice in experimental antiphospholipid syndrome (APS). The content of living, apoptotic and necrotic cells in blood leukocytes was evaluated. Apoptosis in cells was detected using Annexin V conjugated to GFP and propidium iodide. ROS in blood leukocytes were detected using 2',7'-dichlorofluorescein diacetate. The redistribution between the leukocytes populations was assessed by the magnitude of direct (FS) and lateral (SS) light scattering on the flow cytofluorimeter. It was established that the APS reduced the viability of blood leukocytes compare to the control. It is likely that their death is due partly to the activation of apoptosis. In the animals with APS a redistribution between the two main types of leukocytes (granulocytes and agranulocytes) was found out. An increase in the number of granulocytes in the blood was evidenced in cases of APS. It was established that the basal level of ROS production in granulocytes reduced by 27% and in agranulocytes - by 19% compare to the control. Thus, taking into account the attained results it can be argued that in the pathobiochemical mechanisms of APS development the enhanced activation of apoptosis and deficient formation of ROS is significant.