Introduction: Neuroinflammation is the main factor of secondary brain injury following traumatic brain injury (TBI). At the same time, neural cells are most sensitive to damaging factors. The effectiveness of therapeutic approaches to treat neuroinflammation is limited. This study aims to identify new strategies for regulating neuroinflammation in TBI.

Methods: The effect of experimental therapy with sympatholytic reserpine on the expression of M1 and M2 microglial markers (Iba1, iNOS, CD206), the mature neuron marker (NeuN), and the expression of the apoptotic marker Caspase-3 by neurons and microglia in the motor cortex and subventricular zone (SVZ) of ICR mice with TBI was studied using the immunohistochemical method.

Results: Reserpine reduced the number of Iba1⁺ microglia, including polarized M1 microglia, and Caspase-3⁺ microglia in the motor cortex and SVZ of mice with TBI. Reserpine also reduced the number of polarized M2 microglia in the SVZ. However, experimental therapy did not affect the content of NeuN⁺ cells, including NeuN⁺Caspase-3⁺ cells, in the motor cortex and SVZ of mice with TBI.

Conclusion: Sympatholytic reserpine may be a promising compound for developing a new approach to combating neuroinflammation in TBI. We believe that additional administration of drugs that stimulate the differentiation of neural progenitor cells may promote nerve cell regeneration.