INVESTIGATION OF MOLECULAR MECHANISM ON ISCHEMIC

缺血的分子机制研究

• 批准号: 08671576
• 负责人: ISHIKAWA Masatsune
• 金额: $ 1.47万
• 依托单位: TAZUKE-KOFUKAI MEDICAL RESEARCH INSTITUTE (1997)Kyoto University (1996)
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 1996
• 资助国家: 日本
• 起止时间: 1996 至 1997
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-08671576/
• 关键词: cerebral ischemia; apoptosis; spredding depression; ischemic tolerance; necrosis; spreading depression; 能虚血

1)Effect on brain energy metabolismExperimantal study using adult rats revealed that loading of single spreading depression (SD) cause local acidosis in the cortex stimulated directly., followed by it extension into the ipsilateral whole hemisphere. This change was recooverd 20 minutes after stimulation. ATP histochemistry showed same change as that of tissue pH change. The repetitive loading for 120 minutes caused acidosis and ATP depletion for- 45 minutes, which was recovered 60 minutes after stimulation. Thereafter, no change could induced up to six hours later.2)Effect on apoptosisApotosis in the cerebral cortex induced by cerebral ischemia was suppressed by preloading of SD.In contrast, necrosis in the cerebral corrtex was not suppredded.3)Effect on calcium homeostasisNo calcium ion change was observed histochemically on SD loading.Thus, present study revealed that SD protected apoptotic cell death in the cerebral cortex induced by cerebral ischemia.

1)对脑能量代谢的影响成年大鼠的实验研究表明，单次扩散性抑制（SD）负荷可引起直接刺激皮层的局部酸中毒，随后延伸至同侧整个半球。刺激后20分钟，这种变化被重新覆盖。ATP组织化学显示与组织pH变化相同的变化。重复负荷120分钟引起酸中毒和ATP耗竭约45分钟，刺激后60分钟恢复。2）对凋亡的影响SD预负荷可抑制脑缺血诱导的大脑皮层细胞凋亡，但不能抑制大脑皮层细胞坏死。3）对钙稳态的影响SD预负荷后，组织化学上未观察到钙离子的变化。本研究表明，SD保护脑缺血诱导的大脑皮层细胞凋亡。