Antiphospholipid syndrome (APS) is an autoimmune disease that is characterized by arterial or venous thrombosis, thrombocytopenia. APS is one of the autoimmune causes of pregnancy miscarriages. According to the World Health Organization, the incidence of pregnancy miscarriages in the world is 15-25%. Habitual miscarriage is a multifactorial, genetically determined disease. In 50% of cases of habitual miscarriage the establishment of its cause is not possible. About 80% of unexplained reproductive losses are due to immunological disorders. The pathogenetic mechanisms of pregnancy loss mediated by antiphospholipid antibodies (aPL) are thrombosis, placental dysfunction and local inflammation. The nitric oxide system is one of the significant links in the mechanisms of APS development. The effect of selective inhibitor of aminoguanidine inducible NO synthase on the content of glial fibrillary acidic protein (GFAP) and the level of nitric oxide (NO) synthesis in the cerebellum in cases of APS in the pregnant BALB/c mice have been studied. The experimental animals were divided into 5 groups: the 1st – control; the 2nd – animals with experimental APS, the 3rd – animals with APS and administration of aminoguanidine (10 mg/kg). Aminoguanidine was administered intraperitoneally once a day, on a daily basis for 10 days before fertilization and for 17 days during pregnancy. After APS confirmation (on the 10th day), the females of all groups were mated with the males. The animals were removed from the experiment on the 18th day of pregnancy. Western blot analysis for GFAP in cerebellar samples of the control and experimental groups of mice was conducted as well as the densitometric analysis of immunoreactive zones. The content of NO in the samples was determined by the number of its stable metabolites of nitrite anions (NO2¯) and nitrate anions (NO3¯). During the studies, a 1.9 times increase in GFAP (total) and 12.9 times GFAP (49-37 kDa) in the cerebellum of the APS mice on the 18th day of pregnancy as compared to the control group has been established. The increase in GFAP content in the cerebellum of the BALB/c mice with APS is the evidence of the development of reactive astrogliosis. The increase in the content of stable metabolites of nitric oxide NO2 ¯ by 54% and NO3 ¯ by 65% in the cerebellum of mice with APS was found relative to the control group. With the administration of aminoguanidine in the cerebellum of the pregnant mice with APS, a decrease of GFAP (total) by 26%, GFAP (49-37 kDa) by 89%, NO2 ¯ by 31% and NO3 ¯ by 30% was observed in comparison with the indicators of the group of pregnant animals with APS. Therefore, aminoguanidine has a neuroprotective effect in antiphospholipid syndrome with underlying pregnancy which may be mediated not only by inhibiting the activity of inducible NO synthase but also through other cellular targets.
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