Fig. 10

The P2X7R antagonist BBG inhibited the activation of microglia and the NLRP3 inflammasome. a Representative immunoblots of NLRP3, IL-18, and IL-1β expression in the TNC after treatment with NTG, BBG. b–d Quantification of NLRP3 (b), IL-18 (c), IL-1β (d) expression was relative to those of β-actin. Chronic administration of NTG significantly increased the protein level of the above three indexes. Pretreatment with BBG inhibited the NTG induced expression of NLRP3, IL-18, and IL-1β. n = 6 per group; one-way ANOVA and Tukey’s multiple comparison test; data are presented as mean ± SEM; **p < 0.01, ***p < 0.001 compared with the SHAM group; ^#p < 0.05 and ^##p < 0.01 compared with the NTG group. e Iba1 immunostaining in the TNC following NTG and BBG treatment. Scale bar: 20 μm. f Magnified images (× 400 magnification) of Iba1 in the areas of the white dotted line frame in e. g–j Quantification of the Iba1-positive cells (g), Iba1 immunoreactivity (h), total (i), and mean (j) length of processes per microglia. n = 4 per group; 6 sections from each mouse and 4–6 FOV from each section were analyzed; values are expressed as mean ± SEM; one-way ANOVA and Tukey’s multiple comparison test; ***p < 0.001 compared with the SHAM group; ^###p < 0.001 compared with the NTG group