Fig. 3

CB2R activation mitigates neuroinflammation in PD through inhibition of the NLRP3/Caspase-1/IL-1β Pathway. A Detection of protein levels for NLRP3, Caspase-1, pro-Caspase-1, IL-1β, and pro-IL-1β in the midbrain tissue by Western blot, with quantification shown in panels B, C, and D (n = 3). E Immunofluorescence staining for GFAP (green) and NLRP3 (red) in midbrain tissue of mice, with quantification shown in panel F (n = 4). Cells were treated with JWH133 (1 μM) or AM630 (1 μM) for one hour prior to stimulation with 100 μM MPP⁺ for 24 h. G Detection of protein levels for NLRP3, pro-Caspase-1, Caspase-1, IL-1β, and pro-IL-1β in the cells by western blot, with quantification shown in panels H–J (for 3 independent experiments). Cells were treated with JWH133 or AM630 for 1 h prior to incubation with 100 ng/mL LPS for 6 h, and then stimulated with ATP for 30 min before harvesting cell protein. K Detection of protein levels for NLRP3, pro-Caspase-1, Caspase-1, IL-1β, and pro-IL-1β in the cells by western blot, with quantification shown in panels L–N (for 3 independent experiments). O Immunofluorescence staining for GFAP (green) and NLRP3 (red) in astrocytes and the fluorescence intensity statistics of NLRP3 in P (for 3 independent experiments). NS means not significant, ^*P < 0.05, ^**P < 0.01, ^***P < 0.001 compared with the corresponding group, as determined by the one-way ANOVA