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脑缺血预处理不需要 PARP-1。

Brain ischemic preconditioning does not require PARP-1.

机构信息

Department of Pharmacology, University of Florence, Italy.

出版信息

Stroke. 2010 Jan;41(1):181-3. doi: 10.1161/STROKEAHA.109.567826. Epub 2009 Nov 5.

Abstract

BACKGROUND AND PURPOSE

Poly(ADP-ribose) polymerase-1 (PARP-1) is involved in ischemic preconditioning of the heart and cultured neurons, but its role in brain ischemic preconditioning is unknown. Summary of Report- We report that 5-minute bilateral common carotid artery occlusion (BCCAO) in the mouse prompted reduction of infarct volumes triggered 24 hours later by 20-minute middle cerebral artery occlusion (MCAO). Pharmacological PARP-1 inhibition between BCCAO and MCAO did not impair preconditioning. The contents of the PARP-1 substrate NAD, those of its product poly(ADP-ribose), caspase-3 activation, and PARP-1 expression did not change after BCCAO within the preconditioned tissue. PARP-1 KO mice were similarly protected by the 5-minute BCCAO.

CONCLUSIONS

Data demonstrate that, at variance with the heart, PARP-1 is dispensable for brain ischemic preconditioning.

摘要

背景与目的

多聚(ADP-核糖)聚合酶-1(PARP-1)参与心脏和培养神经元的缺血预处理,但它在脑缺血预处理中的作用尚不清楚。 报告摘要:我们报道,在小鼠中进行 5 分钟双侧颈总动脉闭塞(BCCAO)可促使 24 小时后由 20 分钟大脑中动脉闭塞(MCAO)引发的梗死体积减少。在 BCCAO 和 MCAO 之间进行 PARP-1 的药理学抑制不会损害预处理。在预处理组织中,PARP-1 底物 NAD 的含量、其产物多聚(ADP-核糖)的含量、半胱天冬酶-3 的激活和 PARP-1 的表达在 BCCAO 后并未发生变化。PARP-1 KO 小鼠也同样受到 5 分钟 BCCAO 的保护。

结论

数据表明,与心脏不同,PARP-1 对于脑缺血预处理是可有可无的。

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