Abstract
Objectives To investigate the role of Scriptaid in reducing brain injury after intracerebral hemorrhage (ICH) in mice. Methods An ICH model was constructed by injecting autologous blood into the right basal ganglia in mice. The animals were administered 3.5 mg/kg of Scriptaid intraperitoneally after ICH. The hematoma volume and hemoglobin level were measured to examine hematoma resolution. A behavior test and brain edema and white matter injury examinations indicated brain injury after ICH. Results Scriptaid treatment promoted hematoma resolution and reduced the hematoma volume 7 d after ICH compared with the vehicle group (P < 0.05). Scriptaid treatment also alleviated the brain water content in the ipsilateral basal ganglia (P < 0.05) and cortex (P < 0.01) 3 d after ICH. In addition, Scriptaid improved neurological function recovery and alleviated white matter injury 35 d after ICH. Conclusions Scriptaid can protect against brain injury after ICH and may be considered a new medical therapy method for ICH.
Highlights
Intracerebral hemorrhage (ICH) is a fatal subtype of stroke with high morbidity and mortality that accounts for 10%–15% of all strokes [1]
Many previous studies have demonstrated that microglia/microphage polarization is dynamic during a central nervous system injury and modulating microglia/macrophage polarization ameliorates inflammatory injuries after traumatic brain injury (TBI) and ischemic and hemorrhagic strokes [11,12,13]
Many previous studies have described the mechanism of ICH and have attempted to find a therapy, no effective medical treatment for ICH is available at present
Summary
Intracerebral hemorrhage (ICH) is a fatal subtype of stroke with high morbidity and mortality that accounts for 10%–15% of all strokes [1]. Primary brain damage is mainly due to the mass effect and mechanical disruption from extravasated blood. Secondary brain injury is much more complicated and is mainly caused by the physiological response to the hematoma and toxic blood components [2,3,4]. As resident immune cells in the central nervous system (CNS), activated microglia release many inflammatory factors. Many previous studies have demonstrated that microglia/microphage polarization is dynamic during a central nervous system injury and modulating microglia/macrophage polarization ameliorates inflammatory injuries after traumatic brain injury (TBI) and ischemic and hemorrhagic strokes [11,12,13]. Recent studies have demonstrated that activating microglia/macrophages enhances hematoma resolution and improves functional outcomes in a rat model of ICH [14, 15]. Blood-brain barrier (BBB) disruption, which contributes to the development of perihematomal edema, is an important cause of secondary injury after ICH [3, 16]
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