Spinal cord injury (SCI) induces severe motor and sensory dysfunction. We previously showed the neuroprotective effects of COA-Cl, a novel synthesized adenosine analog, in a rat stroke model. In this study, we evaluated the neuroprotective effects of COA-Cl in acute phase of SCI. SCI was induced in rats at the T9 vertebra by using a drop device. Rats were divided into acute and subacute groups. A 5-day dose of 6 mg/kg COA-Cl in saline was given to the acute group immediately after SCI and the subacute group 4 days after SCI. Motor function assessed by Basso-Beattie-Bresnahan scoring and inclined plane test improved significantly in the acute group while the subacute group did not. Histological evaluation and TUNEL staining revealed that both the cavity volume and apoptosis were significantly decreased in the acute group compared with the subacute group. In addition, pERK/ERK was increased in the acute group 7 days after SCI. These results suggest that COA-Cl exerts neuroprotective effects via the ERK pathway when administered in the acute phase after SCI, resulting in the recovery of motor function. COA-Cl could be a novel therapeutic agent for the acute phase of SCI.

脊髓损伤 (SCI) 会导致严重的运动和感觉功能障碍。我们之前在大鼠中风模型中展示了 COA-Cl（一种新型合成腺苷类似物）的神经保护作用。在这项研究中，我们评估了 COA-Cl 在 SCI 急性期的神经保护作用。通过使用下降装置在大鼠的 T9 椎骨处诱导 SCI。大鼠分为急性组和亚急性组。SCI 后立即给予急性组和 SCI 后 4 天的亚急性组 5 天剂量的 6 mg/kg COA-Cl 盐水。通过 Basso-Beattie-Bresnahan 评分和斜面测试评估的运动功能在急性组中显着改善，而亚急性组则没有。组织学评估和 TUNEL 染色显示，与亚急性组相比，急性组的腔体积和细胞凋亡均显着减少。此外，在 SCI 后 7 天，急性组的 pERK/ERK 增加。这些结果表明，当在 SCI 后的急性期给药时，COA-Cl 通过 ERK 途径发挥神经保护作用，导致运动功能的恢复。COA-Cl 可能是 SCI 急性期的新型治疗剂。