Food and Chemical Toxicology 2018-03-26

NBD-BPEA regulates Zn2+- or Cu2+-induced Aβ40 aggregation and cytotoxicity

Tingting Chen, Yuanyuan Zhang, Yanfang Shang, Xuefang Gu, Yue Zhu, Li Zhu

Index: 10.1016/j.fct.2018.03.035

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Abstract

Abnormal interaction of amyloid-β peptide (Aβ) and metal ions is proved to be related to the etiology of Alzheimer's disease (AD). Using metal chelators to reverse metal-triggered Aβ aggregation has become one of the potential therapies for AD. In our work, the effect of metal chelator, NBD-BPEA, on Zn2+- or Cu2+-mediated Aβ40 aggregation and neurotoxicity has been systematically studied. NBD-BPEA exhibits the capability to inhibit the metal-mediated Aβ40 aggregation and disassemble performed Aβ40 aggregates. It also prevents the formation of the β-sheet structure and promotes the reversion of the β-sheet to the normal random coil conformation. Moreover, it can alleviate Zn2+- or Cu2+-Aβ40-induced neurotoxicity, suppress the intracellular ROS and protect against cell apoptosis. These preliminary findings indicate that NBD-BPEA has promising perspective of application in the treatment of AD, and therefore deserve further investigation as potential anti-AD agents.

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