Protective effects of angiotensin receptor control on ischemic neuronal injury

Research Project

Project/Area Number	23592083
Research Category	Grant-in-Aid for Scientific Research (C)
Allocation Type	Multi-year Fund
Section	一般
Research Field	Cerebral neurosurgery
Research Institution	Akita University
Principal Investigator	YANAGISAWA Toshiharu 秋田大学, 医学(系)研究科(研究院), 助教 (20311574)
Co-Investigator(Kenkyū-buntansha)	SUGAWARA Taku 秋田大学, 医学部, 講師 (80241660)
Project Period (FY)	2011 – 2013
Project Status	Completed (Fiscal Year 2013)
Budget Amount *help	¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000) Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000) Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000) Fiscal Year 2011: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Keywords	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
Research Abstract	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.