Abstract
Spinal cord injury (SCI) is a clinical tough neurological problem without efficient cure currently. Blood-spinal cord barrier (BSCB) interruption is not only a crucial pathological feature for SCI process but is a possible target for future SCI treatments; however, few treatments have been developed to intervene BSCB. In the present study, we intravenously injected CO-releasing molecule3 (CORM-3), a classical exogenous CO donor, to the rats experiencing SCI and assessed its protection on BSCB integrity in rats. Our results demonstrated that the exogenous increasing of CO by CORM-3 blocked the tight junction (TJ) protein degeneration and neutrophils infiltration, subsequently suppressed the BSCB damage and improved the motor recovery after SCI. And we certified that the CO-induced down-regulation of MMP-9 expression and activity in neutrophil might be associated with the NF-κB signaling. Taken together, our study indicates that CO-releasing molecule (CORM)-3 ameliorates BSCB after spinal cord injury.
Highlights
Spinal cord injury (SCI) causes longstanding physical and sensory impairment and can be fatal
We initially examined the potential mechanism for CO-regulated matrix metallopeptidases (MMPs)-9 production in neutrophil, which might be associated with NF-kB pathway
Drug and growth factor applications could reduce blood spinal cord barrier (BSCB) damage, the therapeutic efficacy be affected as the restore of BSCB function (Kumar et al, 2016)
Summary
Spinal cord injury (SCI) causes longstanding physical and sensory impairment and can be fatal. Primary injury causes irreversibly local BSCB disruption, which allows the inflammatory cells (primarily neutrophils) infiltrate and migrate into the uninjured section and subsequently exacerbates the secondary sequential damage by secreting neurotoxic factors such as various matrix metallopeptidases (MMPs), reactive oxygen species (ROS), and inflammatory cytokines (Sharma, 2011; Kumar et al, 2016). The genetic or pharmacological suppression of MMP expression and activation or direct blocking the neutrophil infiltration have been demonstrated the protection of BSCB following SCI (Noble et al, 2002; Wells et al, 2003; Yu et al, 2008; Kumar et al, 2016)
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