Figure 3.

Pinocembrin restored cell viability, but did not inhibit amyloid-β peptide (Aβ)1-42 secretion and scavenge intracellular reactive oxygen species (ROS) of human neuroblastoma SH-SY5Y cells overexpressing the Swedish mutant form of human APP (APPsw) in the presence of copper. (A) Neuroprotective effects of pinocembrin evaluated by MTS (3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)- 2-(4-sulfophenyl)-2H-tetrazolium, inner salt) assay. Data are expressed as mean ± SEM, n = 6, ***P < 0.001 vs control, ##P < 0.01, ###P < 0.001 vs copper. (B) Effects of pinocembrin on Aβ1-42 secretion of APPsw cells in the presence of copper. Data are expressed as mean ± SEM, n = 6, ***P < 0.001 vs control. (C,D) Effects of pinocembrin on intracellular ROS generation in APPsw cells in the presence of copper. Intracellular ROS levels were determined based on the 2',7'-dichlorofluorescein (DCF) fluorescence on the ArrayScan high-content screening (HCS) Reader with the Morphology Explorer BioApplication. (a), APPsw group; (b), APPsw cells in the presence of 300 μM copper; (c), APPsw cells in the present of 300 μM copper with pinocembrin treatment at 1.0 μM; (d), 3.0 μM; (e), 10.0 μM. Data are expressed as mean ± SEM, n = 6, **P < 0.01 vs control.

Liu et al. BMC Medicine 2012 10:105   doi:10.1186/1741-7015-10-105
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