Fig. 2

Activation of mGluR5 inhibited α-syn-induced inflammatory signaling. a BV2 cells were transfected with myc-α-syn or vector for 36 h, followed by treatment with CHPG (150 μM) for the indicated time points. The expression of mGluR5, α-syn, and the activities of ERK, JNK, p38, NF-κB p65, and AKT were detected by western blotting. b–d Protein levels of mGluR5 and α-syn were normalized to β-tubulin and β-actin, respectively (b, c). The p-ERK, p-JNK, p-p38, p-NF-κB p65, and p-AKT levels were normalized to the total of ERK, JNK, p38, NF-κB p65, and AKT, respectively (d). Cells transfected with vector without CHPG treatment served as control (a–d). e Primary microglia were infected with LV-NC or LV-α-syn followed by CHPG (150 μM) for different time periods. The expression of mGluR5, α-syn, and the activities of ERK, JNK, p38, NF-κB p65, and AKT were detected by western blotting. f–h Protein levels of mGluR5 and α-syn were normalized to β-tubulin and GAPDH, respectively (f, g). The p-ERK, p-JNK, p-p38, p-NF-κB p65, and p-AKT levels were normalized to the total of ERK, JNK, p38, NF-κB p65, and AKT, respectively (h). Cells infected with LV-NC without CHPG treatment served as control (e–h). Data shown in this figure represent the mean ± SEM (n ≥ 3). The statistical significance was determined by one-way ANOVA followed by Dunnett’s test. **p < 0.01 and ***p < 0.001 versus control (ctr); ^#p < 0.05 and ^###p < 0.001 versus the α-synuclein (α-syn) transfection or LV-α-syn infection without CHPG treatment