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基质金属蛋白酶在全脑缺血后迟发性神经元死亡中的作用。

Involvement of MMPs in delayed neuronal death after global ischemia.

作者信息

Zalewska Teresa, Ziemka-Nałecz Małgorzata, Sarnowska Anna, Domańska-Janik Krystyna

机构信息

Laboratory of Molecular Neuropathology, Department of Neurochemistry, Medical Research Centre, Polish Academy of Sciences, 5 Pawiński St., 02-106 Warsaw, Poland.

出版信息

Acta Neurobiol Exp (Wars). 2002;62(2):53-61. doi: 10.55782/ane-2002-1421.

Abstract

Spatial and temporal relations between metalloproteinase (MMP-2 and MMP-9) activation and laminin degradation in gerbil hippocampus after transient cerebral ischemia has been studied. Activity of MMPs was determined by gelatin zymography in homogenates from dorsal (DP, an equivalent of CA1 sector) and abdominal (AbP, containing CA2-4 and gyrus dentatus) parts of hippocampus. A significant activation of both investigated metalloproteinases was found at 72 h of recovery. Whereas MMP-2 up-regulation did not show any spatial preferences, the increase of MMP-9 activity was observed exclusively in DP. Activation of MMP-9 at this time point correlated spatially with degradation of laminin-protein of extracellular matrix. These results show that MMP pathway may function as a component of delayed neuronal death cascade in the apoptogenic CA1 sector after transient global ischemia.

摘要

研究了沙土鼠短暂性脑缺血后海马中金属蛋白酶(MMP - 2和MMP - 9)激活与层粘连蛋白降解之间的时空关系。通过明胶酶谱法测定海马背侧(DP,相当于CA1区)和腹侧(AbP,包含CA2 - 4和齿状回)部分匀浆中MMPs的活性。在恢复72小时时发现两种研究的金属蛋白酶均有显著激活。MMP - 2上调没有显示出任何空间偏好,而MMP - 9活性增加仅在DP中观察到。此时点MMP - 9的激活在空间上与细胞外基质层粘连蛋白的降解相关。这些结果表明,MMP途径可能作为短暂性全脑缺血后凋亡性CA1区延迟性神经元死亡级联反应的一个组成部分发挥作用。

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