Interactions of Oxidative Stress and Neurovascular Inflammation in the Pathogenesis of Traumatic Brain Injury

摘要: Traumatic brain injury (TBI) is a major cause of death in the young age group and leads to persisting neurological impairment many its victims. It may result permanent functional deficits because both primary secondary damages. This review addresses role oxidative stress TBI-mediated damages by affecting function vascular unit, changes blood-brain barrier (BBB) permeability, posttraumatic edema formation, modulation various pathophysiological factors such as inflammatory enzymes associated with trauma. Oxidative plays pathophysiologic that occur after TBI. In fact, occurs when there an or inability balance antioxidant production reactive oxygen species (ROS) nitrogen (RNS) levels. ROS directly downregulate proteins tight junctions indirectly activate matrix metalloproteinases (MMPs) contribute open BBB. Loosening vasculature perivascular unit stress-induced activation MMPs fluid channel aquaporins promotes cellular edema, enhances leakiness BBB, progression neuroinflammation. Likewise, activates cytokines growth IL-1β, tumor necrosis factor-α (TNF-α), transforming factor-beta (TGF-β) activating MMPs. another pathway, degradation endothelial factor receptor-2 (VEGFR-2) subsequent elevation cellular/serum VEGF level. The decrease VEGFR-2 increase VEGF-A level apoptosis neuroinflammation via caspase-1/3 IL-1β release.