After traumatic brain injury (TBI), inflammation develops in the CNS, an active participant in which is the complement system. Activated complement fragments initiate inflammation, and subsequently significantly affect the processes of repair and regeneration. The aim of the work is to reduce neuroimmune disorders after experimental TBI by blocking excessive inflammation in the early stages of traumatic disease with monoclonal antibodies to the C3 component of complement. The work was carried out on 65 male Wistar rats using the “falling weight” model. To correct neuroinflammation, a preparation of a recombinant monoclonal antibody 3A8, specific for the C3 neodeterminant of the rat complement component, blocking the activation of the alternative complement pathway was administered (i.v., 100 mg/kg). As a reference drug, a recombinant human interleukin-1 receptor antagonist (rIL-1RA) was used, which was administered s.c. (dose of 50 mg/kg). Both drugs were administered once after 30 min of TBI (mode 1) or 24 hours after TBI (mode 2). We studied the levels of corticosterone in the blood, the cytotoxic and proliferative activity of lymphocytes, and behavioral responses in the “plus maze” test. The obtained data indicate that on the 7th day after TBI in rats treated with 3A8 antibodies in mode 1, post-traumatic weight loss was decreased, the natural cytotoxicity of splenocytes and their proliferative activity were increased, and motor and exploratory activity were increased with a significant decrease in the level of anxiety. The introduction of rIL-1RA in these regimens, as well as the combined use of both drugs, did not have a significant effect on the studied parameters.
После черепно-мозговой травмы