Fig. 6: Suppression of p38 MAPK inhibited M1 microglia polarization and alleviated dopaminergic neuron degeneration in Kir6.1-deficent mice of Parkinson’s disease model.

a–d SB203580 reduced the expression of TNF-α (a, c), IL-1β (b) and IL-6 (d) were assessed by qPCR or ELISA in Kir6.1- knockdown microglia. e SB203580 reduced the expression of CD16/32 in Kir6.1 knockdown microglia. f–i SB203580 suppressed the phosphorylation of p38, IKK and p65 in Kir6.1 knockdown microglia. Representative immunoblot (f) and quantitative analysis of the phosphorylation of p38 (g), IKK (h) and p65 (i) in microglia. Data are presented as mean ± SEM from four independent experiments, **p < 0.01, ***p < 0.001 versus corresponding control; ^#p < 0.05, ^##p < 0.01 versus corresponding LPS+INF-γ groups. j-k SB203580 attenuated microglia activation and dopaminergic neuron loss in Kir6.1^+/− mice of lipopolysaccharide-induced Parkinson’s disease model. Microphotographs and stereological counts of IBA-1-positive cells (j) and TH-positive neurons (k) in the substantia nigra compacta. Data are presented as mean ± SEM, ***p < 0.001 versus corresponding control (saline) group; ^#p < 0.05, ^##p < 0.01 versus LPS-treated Kir6.1^+/+ groups; ^$p < 0.05, ^$$p < 0.01 versus LPS-treated Kir6.1^+/- groups. n = 4 for each group