Aβ does not induce oxidative stress in human cerebrovascular smooth muscle cells
Aβ does not induce oxidative stress in human cerebrovascular smooth muscle cells
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DOI：
10.1097/00001756-200207190-00019
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发表时间：
2002-07-19
期刊：
影响因子：
1.7
通讯作者：
Van Nostrand, WE
中科院分区：
文献类型：
--
作者：
Jung, SS;Van Nostrand, WE
我们研究了氧化应激是否参与了致病性Abeta诱导的培养人脑血管平滑肌（HCSM）细胞的退行性机制，HCSM细胞与脑淀粉样血管病（CAA）密切相关。使用细胞可渗透染料二氯荧光素二乙酸酯的研究表明，在暴露于致病性Abeta的HCSM细胞中没有强烈检测到自由基。此外，通过二硝基苯腙和二酪氨酸部分的存在所指示的氧化修饰的蛋白质的检查证明，在致病性Abeta处理的和未处理的HCSM细胞之间没有明显的差异。这些发现支持致病性Abeta诱导的HCSM细胞和神经元细胞中的毒性通过不同的机制发生的观点。
We investigated whether oxidative stress participates in the pathogenic Abeta-induced degenerative mechanism of cultured human cerebrovascular smooth muscle (HCSM) cells, which are intimately involved in cerebral amyloid angiopathy (CAA), Studies using the cell-permeable dye dichlorofluorescein diacetate suggested that free radicals were not robustly detected in HCSM cells exposed to pathogenic Abeta. Furthermore, examination for oxidatively modified proteins, indicated by the presence of dinitrophenylhydrazone and dityrosine moieties, demonstrated no appreciable difference between pathogenic Abeta-treated and untreated HCSM cells, These findings support the notion that pathogenic Abeta-induced toxicity in HCSM cells and neuronal cells occurs by different mechanisms.