Dexmedetomidine reduces inflammation in traumatic brain injury by regulating the inflammatory responses of macrophages and splenocytes.

Traumatic brain injury (TBI) affects people in all demographics, since it is associated with a variety of chronic degenerative diseases, such as Alzheimer's and Parkinson's disease. In TBI, the central nervous system elicits an immune response involving various immune cells that is necessary for healing and defending the body against pathogens, but can also cause secondary damage to the brain if the response is prolonged. In our clinical practice, it has been identified that administration of dexmedetomidine was associated with reduced production of inflammatory cytokines in patients with TBI, which led to the hypothesis that dexmedetomidine may regulate certain inflammatory responses. To test this hypothesis, the roles of dexmedetomidine in the immune system of mice were investigated. Different biological assays were used to assess the influence of dexmedetomidine on the production of inflammatory cytokines, including tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, IL-8 and IL-1 beta. To understand how dexmedetomidine affects different types of immune cells, the influence of dexmedetomidine on splenocytes was also investigated. Finally, the effects of dexmedetomidine on macrophage activation and inflammatory functions were studied. In the present study, clinical observations and in vivo results using a mouse model of TBI revealed the regulatory functions of dexmedetomidine in TBI-associated immune response.