Fig. 3 | Nature Communications

Fig. 3

From: Galectin-3 is required for the microglia-mediated brain inflammation in a model of Huntington’s disease

Fig. 3

Inhibition of the NFκB pathway reduces the abnormal up-regulation of Gal3. a, b Primary microglia harvested from R6/2 mice and their littermate controls (WT) were cultured for 24 h and then treated with Bay11-702 (3 µM) or vehicle (0.1% DMSO) as indicated for 24 h and were then fixed for immunofluorescence staining of Gal3 (green), IbaI (gray), and p65 (red). Nuclei were stained with Hoechst (blue). The localization of nuclei in the right-most panels is outlined by dotted lines. The color bars labeled p65 intensity represent the level of p65 intensity, from low to high fluorescence signals (blue → red, respectively). c An NFκB transcription factor assay was performed on the nuclear extracts prepared from the indicated primary microglia (n = 4). d ELISA was performed on the supernatants collected from the indicated primary microglia to measure the levels of IL1β, IL6, TNFα, and IL10 released by the cells. One dot represents the mean value of each sample. e The levels of nitrite (NO) in the supernatants were measured using the Griess reagent (n = 5). The results were analyzed by two-way ANOVA followed by Tukey’s post hoc test. Data are presented as the means ± SEM. *Specific comparison between WT and R6/2 cells of the same treatment; #Specific comparison between the Bay11-treated and DMSO-treated groups of the same genotype; *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001. Same P-value denotation for #. Scale bar: 10 µm. Source data is available as a Source Data File

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