Therapeutic hypothermia effectively reduces elevated extracellular ascorbate concentrations caused by acute spinal cord injury.
Therapeutic hypothermia effectively reduces elevated extracellular ascorbate concentrations caused by acute spinal cord injury.
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低温治疗可有效降低急性脊髓损伤引起的细胞外抗坏血酸浓度升高。
DOI：
10.1080/21691401.2018.1541136
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发表时间：
2018
期刊：
影响因子：
--
通讯作者：
Zhou Fang
中科院分区：
文献类型：
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作者：
Zhang Yawen;Lv Yang;Ji Wenliang;Zhou Rubing;Gao Shan;Zhou Fang
近年来，全身低温因其在脊髓损伤（SCI）研究领域的应用而受到关注，但详细的分子机制仍不完全清楚。在本研究中，我们使用在线电化学系统（OECS）在体内连续监测大鼠脊髓的抗坏血酸。我们发现大鼠脊髓中抗坏血酸的基础水平为1.85±0.88μmol L−1(n=20)。 SCI后立即升高，损伤后60分钟达到2.36±0.65μmol L−1（基础水平的164.90%±7.99%）（n= 5）。损伤后治疗性低温（28°C）明显减弱了 SCI 诱导的细胞外抗坏血酸增加，并且在 SCI 后 60 分钟，抗坏血酸恢复到 3.01±±0.59μmol L−1（基础水平的 100.24%±5.02%）（n=±5）。这些结果充分表明，用于抗坏血酸检测的 OECS 可以作为了解脊髓损伤期间病理变化的平台。这项研究为抗坏血酸在 SCI 中的重要作用提供了实验证据，可以作为 SCI 的生物标志物。我们的研究结果还提出了低温治疗可以在 SCI 急性期有效发挥神经保护作用的可能性。
In recent years, systemic hypothermia has taken the spotlight for its use in spinal cord injury (SCI) research fields, but detailed molecular mechanisms are still not fully understood. In this study, we use an online-electrochemical system (OECS) to in vivo continuously monitor the ascorbate of the rats’ spinal cord. We find that the basal level of ascorbate in rat spinal cord is 1.85 ± 0.88 μmol L−1(n= 20). It increased immediately after SCI and reached 2.36 ± 0.65 μmol L−1(164.90% ± 7.99% of the basal level) (n= 5) at 60 min after the injury. The SCI-induced extracellular ascorbate increase is obviously attenuated by therapeutic hypothermia (28 °C) after injury and ascorbate returns to 3.01 ± 0.59 μmol L−1(100.24% ± 5.02% of the basal level) (n= 5), at 60 min after SCI. These results substantially manifest that the OECS for ascorbate detection could be employed as a platform for understanding the pathological changes during spinal cord injury. This study provides experimental evidence for the essential roles of ascorbate in SCI which could serve as a biomarker for SCI. Our findings also raise the possibility that therapeutic hypothermia can effectively exert neuroprotection in the acute phase of SCI.