Ramipril protects from free radical induced white matter damage in chronic hypoperfusion in the rat
Ramipril protects from free radical induced white matter damage in chronic hypoperfusion in the rat
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DOI：
10.1016/j.jocn.2006.12.003
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发表时间：
2008-02-01
影响因子：
2
通讯作者：
Kim, Yeong-In
中科院分区：
文献类型：
--
作者：
Kim, Joong-Seok;Yun, Injin;Kim, Yeong-In
我们研究了血管紧张素转换酶抑制剂雷米普利是否可以减轻大鼠慢性灌注不足引起的白质病变，以及氧化应激的抑制是否与由此产生的神经保护有关。雷米普利治疗组显示出显着的保护作用，防止视束、前连合、胼胝体、内囊和尾壳核白质病变的发展。与载体治疗组相比，雷米普利组的丙二醛（MDA）水平和氧化型谷胱甘肽（GSSG）/总谷胱甘肽（GSH(t)）比率也显着降低。这些结果表明，雷米普利由于其对自由基清除的作用，可以预防慢性缺血引起的白质病变。治疗脑血管供血不足状态和血管性痴呆的疗效值得进一步研究。 (c) 2006 Elsevier Ltd. 保留所有权利。
We investigated whether the angiotensin converting enzyme inhibitor, ramipril, could attenuate white matter lesions caused by chronic hypoperfusion in the rat, and whether suppression of oxidative stress is involved in the resulting neuroprotection. The ramipril treatment group showed significant protection from development of white matter lesions in the optic tract, the anterior commissure, the corpus callosum, the internal capsule and the caudoputamen. The level of malondialdehyde (MDA) and the oxidized glutathione (GSSG)/total glutathione (GSH(t)) ratio was also significantly decreased in the ramipril group compared to the vehicle-treated group. These results suggest that ramipril can protect against white matter lesions that result from chronic ischemia due to its effects on free radical scavenging. Further efficacy should be studied in the treatment of cerebrovascular insufficiency states and vascular dementia. (c) 2006 Elsevier Ltd. All rights reserved.