The strategy of modulation for epigenetics against ischemic spinal cord injury

我们研究抑制组蛋白去乙酰化（HDAC）是否对小鼠脊髓缺血后迟发性截瘫具有神经保护作用。治疗组根据HDAC治疗的持续时间（脊髓缺血前7天、缺血前3天、缺血前1天）分为3组。生理盐水治疗组为对照组。我们的实验结果表明，与对照组相比，任何接受HDAC抑制治疗的动物的神经预后都没有明显改善。组织病理学和免疫组织病理学分析也未能显示各组之间的任何差异。根据我们的数据，在小鼠脊髓缺血模型中，HDAC的调节不太可能与脊髓腹角延迟性神经退行性变有关。

We investigated whether inhibition of histon-deacetylation (HDAC) can exert neuroprotective effect against delayed paraplegia after spinal cord ische mia in mice. Treatment groups were divided into 3 groups in corresponding to duration of HDAC treatment (7 days before, 3 days before, and 1 day before spinal cord ischemia). Saline treatment was defined as control group. As a result from our experiments, any animal treated with inhibition of HDAC could not show significantly improve neurological outcome in comparison with control group. Histopathological and immunohistopathological analysis also failed to show any differences among all groups. According to our data, modulation of HDAC is unlikely to be associated with delayed neurological degeneration in spinal ventral horn in mice spinal cord ischemic model.