Research of the functional activity of immunocompetent brain cells on separate occasions after experimental traumatic brain injury
DOI:
https://doi.org/10.25305/unj.205793Keywords:
brain injury, microglia, brain macrophages, phagocytosis, experimental studiesAbstract
Objective: To investigate the functional activity of microglia and monocytic/macrophage cells on separate occasions after the rat model of experimental brain injury.
Materials and methods. The rat model of experimental brain injury was simulated by dropping a load weighing 100 g from a height of 120 cm. Microglia and infiltrating CNS monocytes were isolated from rat brain tissue in a stepwise Percoll cushion. The activity of phagocytic brain cells was determined in the HCT test by the spectrophotometric method. Myeloperoxidase activity was determined in cell lysate by a quantitative spectrophotometric method.
Results. It was found that after brain injury there is an increase in the number of microglial / monocyte cells and an increase in spontaneous production of toxic oxygen molecules by these cells, which depends on the duration of injury and the location of the injury. The greatest threefold increase in microglial and monocytic/macrophage cells is determined on the 5th day after brain injury in the hemisphere with a traumatic injury. The maximum increase in spontaneous production of superoxide anion radical by these cells is also determined on the 5th day after brain injury. In contrast, myeloperoxidase activity of this cell population increases as early as 24 h after brain injury and gradually decreases to control values on the 10th day after the injury, which indicates the gradual development of the process.
Conclusion. The result of the researches demonstrated that on the 5th day after brain injury microglial and monocytic/macrophage M1 cells of pro-inflammatory phenotype prevail in the inflammation site. Influences on the cellular and molecular mechanisms that regulate the functional responses of microglia/macrophages after brain injury may facilitate the development of future therapeutic interventions aimed at the phenotypic transition of these cells from M1 to M2, which is necessary to improve CNS recovery.
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