Intervention of neuroinflammation in the traumatic brain injury trajectory: In vivo and clinical approaches

•Traumatic brain injury (TBI) happens due to motor vehicle accidents, the building falls, and injuries.•Neuroinflammation is caused by TBI and can aggravate the progression of tissue deterioration.•TBI increase the production of brain-derived neurotrophic factors.•TBI pathogenesis is associated with NOX, a class of enzymes whose sole function is to generate ROS. TBI has been one of the top causes of death and morbidity worldwide, yet despite enormous efforts to discover neuroprotective therapeutics for this serious disease, no beneficial outcomes in human clinical trials have been reported to date. Traumatic brain injury (TBI) can occur as a result of any type of trauma, from a simple hit to the head to a penetrating injury to the brain. TBI causes delayed secondary damage events as a result of neurochemical, metabolic, and cellular alterations that account for many of the neurological impairments reported following TBI. We focus on the ability of soluble and cellular inflammatory mediators to promote repair and regeneration versus secondary injury and neurodegeneration in our discussion, which is structured around the kinetics of the immune response to TBI — from immediate triggers through chronic neuroinflammation. Neuroinflammation is caused by traumatic brain injury and can aggravate the progression of tissue deterioration. Immune cells respond acutely to signals from injured cells, develop neuroinflammation, and eventually cause pathology. So neuroinflammation and the immune system could be a target for TBI treatment. However, there are various approaches to the treatment of TBI. This review will provide the literature-based modulation of receptors, ion channels, transporters, and enzymes to attenuate traumatic brain injury.