活力测定
细胞毒性
SH-SY5Y型
化学
台盼蓝
细胞培养
分子生物学
MTT法
神经母细胞瘤
药理学
细胞
生物化学
生物
体外
遗传学
作者
Kenta Fukui,Kazuma Yachi,Hidemi Yoshida,Kunikazu Tanji,Tomoh Matsumiya,Ryo Hayakari,Kazushi Tsuruga,Hiroshi Tanaka,Tadaatsu Imaizumi
标识
DOI:10.1016/j.neures.2017.05.005
摘要
Amyloid-beta (Aβ) peptides, Aβ 1–42 (Aβ42) and Aβ43, in particular, have been implicated in the pathophysiology of neurodegenerative disease such as Alzheimer’s disease (AD). Rebamipide (REB), a gastrointestinal protective drug, can cross the blood-brain barrier after oral administration; however, the effects of REB on neuronal cells have not yet been reported. In this study, we investigated the effects of REB on Aβ43-induced cytotoxicity (monomers, 10 μM) in cultured SH-SY5Y human neuroblastoma cells. Addition of REB (10–1000 nM) into the media partially ameliorated the reduced cell viability observed after Aβ43 treatment, which was determined by the MTT assay. REB reduced the levels of intracellular Aβ oligomers (100–150 kDa) that were formed from the exogenous addition of Aβ43 monomers. In addition, REB (30 nM) reduced endogenous Aβ42 secretion, which was analyzed by the enzyme-linked immunosorbent assay. Furthermore, REB enhanced the expression of tumor necrosis factor-α-converting enzyme/a disintegrin and metalloproteinase-17, neprilysin, matrix-metalloproteinase-14 (MMP-14)/membrane type-1 MMP, cyclooxygenase-2, and sirtuin 1, even in cells challenged with Aβ43. These results suggest that REB improves the cell viability by inducing genes that regulate Aβ levels and also genes that are cytoprotective. The secondary use of REB may have potential in the prevention of Aβ-mediated diseases, particularly AD.
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