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Fig. 3 | Journal of Neuroinflammation

Fig. 3

From: The neuroprotective N-terminal amyloid-β core hexapeptide reverses reactive gliosis and gliotoxicity in Alzheimer’s disease pathology models

Fig. 3

N-Aβcore co-treatment attenuates Aβ1–42-induced increases in proinflammatory markers in BV2 cells. BV2 cells were treated daily for 5 days with media only (Control), 500 nM Aβ1–42, 500 nM Aβ1–42 + 500 nM N-Aβcore or 500 nM Aβ1–42 + 500 nM SEVAAQ (inactive substituted N-Aβcore) or daily for 6 days with 500 nM Aβ1–42 under the reversal conditions (see Fig. 6A, legend). A Representative images of immunostaining for TNFα (top) and iNOS expression (bottom) in BV2 cells. Images obtained using a 63X objective on a Leica TCS SP8 confocal microscope. Scale bar: 50 μm. B Quantification of TNFα (n = 3) and D iNOS (n = 3) fluorescence intensities in A. Data shown as means ± 95% confidence intervals. C Quantification of IL-1β release into the BV2 cell culture media via ELISA after treatment as described above. Data shown as means ± SD. All data in BD analyzed via one-way ANOVA with Dunnett post hoc test as compared to Aβ1–42. **p < 0.01; ***p < 0.001; ****p < 0.0001. Rev reversal condition

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