| Literature DB >> 32209125 |
Krystal Sotolongo1, Jorge Ghiso2,3, Agueda Rostagno4.
Abstract
After the publication of this article [1], we became aware that there were errors in Figs. 4 and 31.Entities:
Year: 2020 PMID: 32209125 PMCID: PMC7093983 DOI: 10.1186/s13195-020-00605-6
Source DB: PubMed Journal: Alzheimers Res Ther Impact factor: 6.982
Fig. 4Methazolamide, melatonin, and Trolox protect from Aβ-mediated ROS generation in SH-SY5Y. Following 24 h incubation with Aβ42 (0–25 μM) in the presence or absence of MTZ (300 μM), MEL (100 μM), and Trolox (300 μM), ROS-generated species were detected with CellROX 5 μM), and nuclei counterstained with Hoechst (1 μg/ml). Images depict CellRox fluorescence (red signal) and DAPI DNA counterstaining; bar, 25 μm. The graph on the right illustrates the quantitation of CellROX fluorescence values normalized to DAPI signal using ImageJ analysis software; data is represented as mean ± SEM. **p < 0.01 and ***p < 0.001
Fig. 13Methazolamide, melatonin, and Trolox activate Nrf2 through a PI3K-mediated pathway. SH-SY5Y cells were treated with MTZ (300 μM), MEL (100 μM), or Trolox (300 μM) in the presence of the PI3K inhibitors LY294002 and Wortmannin (10 μM each) or the GSK-3 inhibitor SB216763 (10 μM). As a control, cells were incubated with SFN (5 μM), a compound capable of activating Nrf2 through disruption of its binding to Keap-1, a PI3K-independent pathway. In all cases, Nrf2 expression was evaluated by immunocytochemistry as in Figs. 7 and 8. Green fluorescence highlights Nrf2 nuclear translocation, and red fluorescence depicts actin staining with Alexa 588-conjugated phalloidin. Bar represents 20 μm in all images. Quantitation of the nuclear fluorescence signal is shown in Additional file 2: Figure S2