The strategy of modulation for epigenetics against ischemic spinal cord injury

表观遗传学调控缺血性脊髓损伤的策略

• 批准号: 22591548
• 负责人: SAIKAWA Satoko
• 金额: $ 2.91万
• 依托单位: University of the Ryukyus
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2010
• 资助国家: 日本
• 起止时间: 2010 至 2012
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-22591548/
• 关键词: 硫化水素; 遅発性対麻痺; 脊髄虚血; アポトーシス; 遅発性麻痺; エピジェネティクス; 神経変性; 虚血性脊髄障害; 対麻痺; ヒストン脱アセチル化酵素; 脊髄運動神経細胞

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.

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。

项目成果

遅発性対麻痺にカスパーゼ3は必須である

Caspase-3 对于迟发性截瘫至关重要

• 发表时间: 2011
• 作者: Kakinohana M;et al;垣花学
• 通讯作者: 垣花学

Delayed paraplegia after spinal cord ischemic injury requires caspase-3 activation in mice.

• DOI: 10.1161/strokeaha.110.600429
• 发表时间: 2011-08
• 期刊: Stroke
• 影响因子: 8.3
• 作者: Kakinohana M;Kida K;Minamishima S;Atochin DN;Huang PL;Kaneki M;Ichinose F
• 通讯作者: Ichinose F

Delayed paraplegia after spinal cord ischemic injuries requires caspase-3 activation in mice

小鼠脊髓缺血损伤后迟发性截瘫需要激活 caspase-3

• 发表时间: 2011
• 期刊: Stroke
• 影响因子: 8.3
• 作者: M Kakinohana(研究分担者);K Kida;S Minamishima;DN Atochin;PL Huang;M Kaneki;F Ichinose
• 通讯作者: F Ichinose