Free -radical generation by amyloid p protein and the protective effect by laminin against amyloid β-protein induced toxicity

淀粉样p蛋白产生自由基以及层粘连蛋白对淀粉样β蛋白诱导的毒性的保护作用

基本信息

批准号：
15591235
负责人：
HAYASHI Yoshihito
金额：
$ 1.92万
依托单位：
University of Miyazaki (2004)宮崎医科大学 (2003)
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2003
资助国家：
日本
起止时间：
2003 至 2004
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-15591235/
关键词：
β amyloid laminin free radical NMDA

项目摘要

We investigated the inhibitory effect by laminin, which is one of the extracellular matrix components, against beta amyloid(Aβ) induced free radicals by electron paramagnetic resonance(EPR) using PC12 cells with two kinds of spin trap, 5,5-dimethyl-1-pyrroline-N-oxide ; DMPO, α-(4-pyridyl-1-oxide)-N-tert-butylnitrone ; POBN respectively. We investigated two kinds of experiment to clear the mechanism how laminin shows the protection against Aβ. At first, EPR measurement was performed to see whether or not laminin directly inhibit Aβ induced free radicals, Aβ was mixed with laminin and the solution was added to PC12 cells. The second, EPR measurement was also performed to see whether or not the cells which attached laminin get strengthened their defense function.The free radical production was reduced when Aβ was mixed with laminin and the cell viability also increased compared with Aβ only added to the cells, though there was no difference in generating free radicals between cells which were attached with laminin for 24hrs before Aβ addition and cells which did not attach laminin for 24hrs. Therefore we concluded that laminin has neuroprotective ability and its protective effect against Aβ induced free radical generation is due to possibly direct reaction with Aβ.

我们研究了层粘连蛋白的抑制作用，层粘连蛋白是细胞外基质成分之一，使用β淀粉样蛋白（Aβ）诱导的β淀粉样蛋白（Aβ）诱导的自由基通过电子顺磁共振（EPR）使用PC12细胞，该pc12细胞使用具有两种旋转诱捕器，5,5-二氨基-1-二甲基-1-二甲基-1-吡咯烷基 - N-氧化物； DMPO，α-（4-吡啶基-1-氧化物）-N-TERT叔丁基硝酸； POBN分别。我们研究了两种实验，以清除层粘连蛋白如何显示对Aβ的保护的机制。首先，进行了EPR测量，以查看层粘连蛋白是否直接抑制Aβ诱导的自由基，Aβ与层粘连蛋白混合，并将溶液添加到PC12细胞中。还进行了第二个EPR测量，以查看附着的层粘连蛋白的细胞是否增强了其防御功能。当Aβ与层粘连蛋白混合并增加了细胞活力时，自由基产生降低。与仅添加到细胞中的Aβ相比，尽管在与层粘连蛋白相连的细胞之间没有差异，但在Aβ添加之前与层粘连蛋白相连，而细胞和未在24小时内未连接层粘连蛋白的细胞。因此，我们得出的结论是，层粘连蛋白具有神经保护能力，其针对Aβ诱导的自由基产生的保护作用是由于可能与Aβ的直接反应所致。