The Journal of Neurobehavioral Sciences
Yazarlar: Alexander A. Nefodov , Igor F. Belenichev , Elena A. Nefodova , Nina V. Bukhtiyarova , Sergii V. Levich , Sergii N. nov
Konular:-
DOI:10.5455/JNBS.1525619232
Anahtar Kelimeler:-
Özet: Multiple sclerosis is a multifactorial, autoimmune, chronic inflammatory demyelinating disease of the central nervous system. Recent studies do not give possibility to estimate the contribution of neurodegenerative changes in neurological deficit of individual patient, to predict the disease development and the effectiveness of therapy. The goal of our research was to investigate methylprednisolone and citicoline co-administration effect to the processes of energy providing of the mitochondria of the cerebral cortex neurons in experimental allergic encephalomyelitis. Experiments were carried out on rats of both sexes weighing 150180 g. Experimental allergic encephalomyelitis was induced by a single subcutaneous inoculation of encephalitogenic mixture in complete Freund’s adjuvant. As material, we used brains. We studied markers of mitochondrial dysfunction and content of adenine nucleotides, lactate, malate, isocitrate, aspartate, pyruvate. We also studied the state of neurons, their area, RNA-content and proportion of apoptotic cells. Formation of experimental allergic encephalomyelitis (EAE) led to permanent disturbance of energy metabolism of brain. The administrations of methylprednisolone did not have a significant effect. Co-administration of methylprednisolone and citicoline exerted significant influence on some parameters of mitochondrial dysfunction and brain energy metabolism. We also found neuronal damage of sensorimotor cortex of experimental animals and to the neuroapoptosis activation. Administration of methylprednisolone resulted in direct neuroprotective effect. Combination of citicoline and methylprednisolone limit activity of unproductive anaerobic glycolysis and increases aerobic ATP synthesis reaction. Thus, the combination of citicoline and methylprednisolone does not affect the activity of malate aspartatic shunt in EAE conditions.