The Research of Intracellular Energy-Related Metabolic Regulatory Enzymes on Delayed Neuronal Cell Death

细胞内能量相关代谢调节酶对神经细胞迟发性死亡的研究

• 批准号: 20591806
• 负责人: FUKUDA Shiro
• 金额: $ 2.83万
• 依托单位: Yamaguchi University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2008
• 资助国家: 日本
• 起止时间: 2008 至 2010
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-20591806/
• 关键词: AMP-activated Protein Kinase; 脳虚血; ラット; AICAR; compound C; AMP-activated rotein kinase; 細胞内エネルギー調節; 前脳虚血; 海馬; 遅発性神経細胞傷害; AMP-ativated protein kinase; 中大脳動脈閉塞モデル; TTC染色; 神経細胞傷害; ウィスターラット; 脳・神経; 虚血性細胞障害; 細胞内代謝調節; 免疫ブロット法; ラット断頭モデル; 全脳虚血

The tendency of increasing in p-AMPKα2 and p-AMPKβ1 was observed in the brain samples 60 minutes after decapitation of rats. This result suggested that AMPK was activated by neuronal ischemia. Infarction volumes in focal ischemia with rat model were decreased by AICAR, which is one of the activators of AMPK. However, AICAR exacerbated neuronal damage in gerbil forebrain ischemia, and the same exacerbation was observed in the administration of Compound C, one of the AMPK inhibitors.

大鼠斩首后60分钟，在脑样本中观察到P-AMPKα2和P-AMPKβ1增加的趋势。该结果表明AMPK被神经元缺血激活。 AICAR是AMPK的激活剂之一，将局灶性缺血中的违规量减少。然而，AICAR加剧了沙鼠前脑缺血中的神经元损伤，并且在化合物C的给药中观察到了同样的加重，这是AMPK抑制剂之一。

项目成果

Do opioids aggravate ischemic spinal cord injury in rabbits?

阿片类药物会加重兔子缺血性脊髓损伤吗？

• 发表时间: 2008
• 作者: 津田晃祐;三木秀宣;菅野伸彦;ほか;福田 志朗
• 通讯作者: 福田 志朗