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CO-Releasing Molecule (CORM)-3 Ameliorates Spinal Cord-Blood Barrier Disruption Following Injury to the Spinal Cord

机译:共同释放分子(CINT)-3改善脊髓损伤后脊髓瓣膜阻隔破坏

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摘要

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.
机译:脊髓损伤(SCI)是目前没有有效治愈的临床严重的神经系统问题。血脊髓屏障(BSCB)中断不仅是SCI过程的关键病理特征,而且是未来SCI治疗的可能目标;然而,已经开发出少量的治疗来介入BSCB。在本研究中,我们静脉内注射了经典外源CO供体,经典外源CO供体的共同释放分子3(COM-3),并评估了对大鼠BSCB完整性的保护。我们的研究结果表明,COM-3的外源性增加阻断了紧密的结(TJ)蛋白质退化和中性粒细胞浸润,随后抑制了BSCB损伤并改善了SCI后的电动机恢复。并且我们证明了中性粒细胞中的MMP-9表达和活性的共同诱导的下调可能与NF-κB信号传导相关。我们的研究表明,脊髓损伤后共同释放分子(CORM)-3改善BSCB。

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