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自噬参与了缺血预处理。

Autophagy is involved in the ischemic preconditioning.

作者信息

Park Hee-Kwon, Chu Kon, Jung Keun-Hwa, Lee Soon-Tae, Bahn Jae-Joon, Kim Manho, Lee Sang Kun, Roh Jae-Kyu

机构信息

Stroke & Stem Cell Laboratory, Department of Neurology, Clinical Research Institute, Seoul National University Hospital, Seoul, South Korea.

出版信息

Neurosci Lett. 2009 Feb 13;451(1):16-9. doi: 10.1016/j.neulet.2008.12.019. Epub 2008 Dec 16.

Abstract

Autophagy is a key pathway for the clearance of damaged organelles. Ischemic preconditioning (IPC) and autophagy are enhanced by mild hypoxic insults, but the association between autophagy and IPC remains unclear. We investigated the existence and role of autophagy in IPC. In an in vitro PC12 cell model, IPC increased generation and degradation of autophagosomes, as revealed by increased LC3-II bands, cathepsin D positive cells, lysosomal activity and autophagic vacuoles on electron microscopy. Autophagic activity was blocked using 3-methyladenine during IPC, and cell viabilities were measured using FASC and WST-1 assays. Inhibition of autophagy, especially during reperfusion or lethal oxygen-glucose deprivation periods ameliorated the neuroprotective effects of IPC. Moreover, inhibiting autophagy also attenuated Hsp70 upregulation induced by IPC. These findings imply that autophagy participates in IPC-induced neuroprotection, and that autophagy might provide a means of neuroprotection against cerebral ischemia.

摘要

自噬是清除受损细胞器的关键途径。轻度缺氧损伤可增强缺血预处理(IPC)和自噬,但自噬与IPC之间的关联仍不清楚。我们研究了自噬在IPC中的存在及作用。在体外PC12细胞模型中,IPC增加了自噬体的生成和降解,这通过LC3-II条带增加、组织蛋白酶D阳性细胞、溶酶体活性以及电子显微镜下的自噬泡得以揭示。在IPC期间使用3-甲基腺嘌呤阻断自噬活性,并使用FASC和WST-1检测法测量细胞活力。抑制自噬,尤其是在再灌注或致死性氧-葡萄糖剥夺期间,可改善IPC的神经保护作用。此外,抑制自噬也减弱了IPC诱导的Hsp70上调。这些发现表明自噬参与了IPC诱导的神经保护作用,并且自噬可能为对抗脑缺血提供一种神经保护手段。

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