Stroke:增强一种长寿基因 可预防脑梗塞引发的血管性痴呆
日本研究人员在新一期美国《中风》(Stroke)杂志上报告说,他们发现如果让一种长寿基因在脑内更加积极地发挥作用,就可预防脑梗塞引发的血管性痴呆。


日本研究人员在新一期美国《中风》杂志上报告说,他们发现如果让一种长寿基因在脑内更加积极地发挥作用,就可预防脑梗塞引发的血管性痴呆。

血管性痴呆是由缺血性中风、出血性中风等脑血管疾病所致的严重认知功能障碍。

日本国立循环器官疾病研究中心等机构的研究人员报告说,SIRT1是一种去乙酰化酶,与细胞增殖、分化、衰老、凋亡和代谢密切相关。编码这种酶的SIRT1基因被认为是一种长寿基因,能够遏制老化。

研究人员通过基因操作,使实验鼠脑内SIRT1基因的表达增强,进而使SIRT1酶的生成量达到通常水平的2至3倍,然后通过手术使实验鼠的颈动脉变细。

研究人员发现,虽然实验鼠颈动脉变细了,但是脑内血流能够维持在原有水平的90%以上。而普通实验鼠颈动脉变细后,脑内血流则只能维持原有水平的约70%。

研究人员发现,这是由于SIRT1基因表达增强后,能够促使合成一氧化氮的酶保持非常活跃的状态,而一氧化氮能够扩张血管,从而有利于维持脑血流。

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  • Silent Information Regulator 2 Homolog 1 Counters Cerebral Hypoperfusion Injury by Deacetylating Endothelial Nitric Oxide Synthase

    Background and Purpose:Silent information regulator 2 homolog 1 (SIRT1) is a protein deacetylase that has been reported to suppress neurodegenerative and cardiovascular diseases in model organisms. We hypothesized that neurovascular protection is one of the diverse actions of SIRT1. This study was designed to determine whether SIRT1 protects against the consequences of cerebral hypoperfusion in vivo. Methods:Sirt1-overexpressing (Sirt1-Tg) mice driven by a prion promoter and their wild-type littermates were subjected to bilateral common carotid artery stenosis using external microcoils. Using Sirt1-Tg mice, we assessed the effect of SIRT1 on cerebral blood flow, cerebral angioarchitecture, histological and ultrastructural changes, and spatial working memory at several time points. We also evaluated the effects of preadministration of SIRT1 inhibitors or endothelial nitric oxide synthase inhibitors on cerebral blood flow after bilateral common carotid artery stenosis in Sirt1-Tg mice. Levels of acetylated and nonacetylated endothelial nitric oxide synthase were measured semiquantitatively with immunoblotting. Results:Cerebral hypoperfusion induced by bilateral common carotid artery stenosis caused memory impairment and histological changes in wild-type littermates. However, these phenotypes were rescued in Sirt1-Tg mice, where cerebral blood flow was maintained even poststenosis. Electron microscopic analyses showed irregularities in the vascular endothelia, such as tight junction openings in wild-type mice, which were absent in Sirt1-Tg littermates. Brain endothelial nitric oxide synthase was acetylated after cerebral hypoperfusion in wild-type littermates but remained unacetylated in Sirt1-Tg mice. Moreover, treatment with SIRT1 inhibitors and endothelial nitric oxide synthase inhibitors abolished the vasculoprotective effects of SIRT1. Conclusions:Our results indicate that neurovascular endothelial SIRT1 potentiation upregulates the nitric oxide system and counters cerebral hypoperfusion injury. This novel cerebral blood flow–preserving mechanism offers potential molecular targets for future therapeutic intervention.

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