Protective effects of angiotensin receptor control on ischemic neuronal injury

血管紧张素受体控制对缺血性神经元损伤的保护作用

• 批准号: 23592083
• 负责人: YANAGISAWA Toshiharu
• 金额: $ 3.33万
• 依托单位: Akita University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2011
• 资助国家: 日本
• 起止时间: 2011 至 2013
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-23592083/
• 关键词: アンジオテンシン受容体; 脳虚血; 神経細胞死; アポトーシス; ＡＲＢ; チトクロームｃ

Mitochondrial apoptosis after cerebral ischemia is known to mediate neuronal injury. Angiotensin II type 1 receptor activation results in production of superoxide, but whether angiotensin II type 1 receptor blockade prevents mitochondrial apoptosis after ischemia remains unclear. Normotensive rats received the angiotensin II type 1 receptor blocker, candesartan or only vehicle before induction of global cerebral ischemia. Approximately 30% of the hippocampal CA1 neurons survived in candesartan-treated animals, whereas only 2% of neurons survived in vehicle-treated animals. Superoxide production and cytochrome c release were significantly less in these vulnerable neurons in candesartan-treated animals than in vehicle-treated animals. Angiotensin II type 1 receptor may have an essential role in apoptotic cell death in vulnerable neurons after global cerebral ischemia.

已知脑缺血后的线粒体凋亡可介导神经元损伤。血管紧张素II类型1型受体激活会导致超氧化物的产生，但是血管紧张素II型1型受体阻断是否可以防止缺血后的线粒体细胞凋亡尚不清楚。正常的大鼠在诱导全球脑缺血之前接受了血管紧张素II类型1型受体阻滞剂，Candesartan或仅载体。大约30％的海马CA1神经元在糖果治疗的动物中存活，而只有2％的神经元在媒介物处理的动物中存活。这些脆弱的神经元中的超氧化物的产生和细胞色素C的释放明显少于在经媒介物处理的动物中，这些脆弱的神经元的生产较少。全球脑缺血后，血管紧张素II类型1型受体在脆弱神经元中的凋亡细胞死亡中可能具有重要作用。