Therapeutic hypothermia effectively reduces elevated extracellular ascorbate concentrations caused by acute spinal cord injury.
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.
['Zhang|Yawen|Y|', 'Lv|Yang|Y|', 'Ji|Wenliang|W|', 'Zhou|Rubing|R|', 'Gao|Shan|S|', 'Zhou|Fang|F|']
D000208:Acute Disease D000818:Animals D001205:Ascorbic Acid D005110:Extracellular Space D007036:Hypothermia, Induced D008297:Male D051381:Rats D017207:Rats, Sprague-Dawley D013116:Spinal Cord D013119:Spinal Cord Injuries
ascorbate spinal cord injury Online electrochemical system in vivo microdialysis