Department of Pharmacology and Molecular Therapeutics, Kumamoto University Graduate School of Medical Sciences, Kumamoto, Japan.
Hypertension. 2011 Oct;58(4):635-42. doi: 10.1161/HYPERTENSIONAHA.111.173534. Epub 2011 Aug 22.
The role of the renin-angiotensin system in cognitive impairment is unclear. This work was undertaken to test our hypothesis that renin-angiotensin system may contribute to cognitive decline and brain damage caused by chronic cerebral ischemia. C57BL/6J mice were subjected to bilateral common carotid artery stenosis with microcoil to prepare mice with chronic cerebral hypoperfusion, a model of subcortical vascular dementia. The effects of aliskiren, a direct renin inhibitor, or Tempol, a superoxide scavenger, on brain damage and working memory in these mice were examined. Chronic cerebral hypoperfusion significantly increased brain renin activity and angiotensinogen expression in C57BL/6J mice, which was attributed to the increased renin in activated astrocytes and microvessels and the increased angiotensinogen in activated astrocytes in white matter. Aliskiren pretreatment significantly inhibited brain renin activity and ameliorated brain p67(phox)-related NADPH oxidase activity, oxidative stress, glial activation, white matter lesion, and spatial working memory deficits in C57BL/6J mice with bilateral common carotid artery stenosis. To elucidate the role of oxidative stress in brain protective effects of aliskiren, we also examined the effect of Tempol in the same mice with bilateral common carotid artery stenosis. Tempol pretreatment mimicked the brain protective effects of aliskiren in this mouse model. Posttreatment of mice with aliskiren or Tempol after bilateral common carotid artery stenosis also prevented cognitive decline. In conclusion, chronic cerebral hypoperfusion induced the activation of the brain renin-angiotensin system. Aliskiren ameliorated brain damage and working memory deficits in the model of chronic cerebral ischemia through the attenuation of oxidative stress. Thus, direct renin inhibition seems to be a promising therapeutic strategy for subcortical vascular dementia.
肾素-血管紧张素系统在认知障碍中的作用尚不清楚。本研究旨在验证我们的假设,即肾素-血管紧张素系统可能导致慢性脑缺血引起的认知下降和脑损伤。通过微线圈双侧颈总动脉狭窄制备慢性脑低灌注小鼠模型,模拟皮质下血管性痴呆。观察直接肾素抑制剂阿利克仑或超氧化物清除剂 Tempol 对这些小鼠脑损伤和工作记忆的影响。慢性脑低灌注显著增加了 C57BL/6J 小鼠脑肾素活性和血管紧张素原表达,这归因于活化星形胶质细胞和微血管中肾素增加以及白质中活化星形胶质细胞中血管紧张素原增加。阿利克仑预处理显著抑制脑肾素活性,并改善双侧颈总动脉狭窄 C57BL/6J 小鼠脑 p67(phox)-相关 NADPH 氧化酶活性、氧化应激、胶质细胞激活、白质病变和空间工作记忆缺陷。为了阐明氧化应激在阿利克仑脑保护作用中的作用,我们还在双侧颈总动脉狭窄的相同小鼠中研究了 Tempol 的作用。Tempol 预处理模拟了阿利克仑在该小鼠模型中的脑保护作用。在双侧颈总动脉狭窄后给予阿利克仑或 Tempol 治疗也可预防认知下降。总之,慢性脑低灌注诱导脑肾素-血管紧张素系统激活。阿利克仑通过减轻氧化应激改善慢性脑缺血模型中的脑损伤和工作记忆缺陷。因此,直接肾素抑制似乎是皮质下血管性痴呆的一种有前途的治疗策略。