The study aims to investigate the infuence of L-arginine on the content of nitrite anions (NO2¯) and nitrate anions (NO3¯) and the content of glial fibrillary acidic protein (GFAP) in the cerebellum and cerebral hemispheres of BALB/c mice with antiphospholipid syndrome.
The studies were performed on 30 female BALB/c mice. The experimental animals were divided into 3 groups: 1 – control (intact) animals; 2 – animals with experimental antiphospholipid syndrome (APS), 3 – animals with APS, which were injected with L-arginine at a dose of 25 mg/kg, intraperitoneally once a day, for 10 consecutive days after the development of APS.
The increase in glial fibrillary acidic protein and stable metabolites of nitric oxide NO2¯ and NO3¯ in the cerebellum and cerebral hemispheres, relative to the control, was observed in APS-developed BALB/c mice. In case of injection of the precursor of NO synthesis, L-arginine, animals with APS were found to have a further significant increase in the content of NO2¯ and NO3¯ in the cerebellum and the cerebral hemispheres. The introduction of L-arginine did not cause significant changes in GFAP (total) in cerebral hemispheres. However, GFAP content (49-37 kDa) was decreasing. The cerebellum showed an increase in GFAP (total) and GFAP (49-37 kDa) content, compared to the performance of animals with APS.
Therefore, the increase in the content of GFAP in the cerebellum and the cerebral hemispheres of BALB/c mice under APS indicates the development of reactive astrogliosis. The introduction of the precursor of NO synthesis, L-arginine, is accompanied by an increase in the content of stable metabolites of nitric oxide (NO2¯, NO3¯) and GFAP in the cerebellum of BALB/c mice, which can indirectly confirm the role of NO in regulating of GFAP expression in astrocytes under APS.
Expression of glial fibrillar acidic protein in the sensorimotor cortex of the cerebral hemispheres in the modeling of transient ischemia against the background of previous sensitization by brain antigen and immunocorrection
