Fig. 5: Kir6.1 inhibited the activation of p38 MAPK and NF-κB in microglia.
From: Kir6.1/K-ATP channel modulates microglia phenotypes: implication in Parkinson’s disease
a–f Kir6.1 knockdown enhanced the phosphorylation of p38, IKK and p65 in microglia treated with LPS+INF-γ. Representative Immunoblot (a) and quantitative analysis of the phosphorylation of p38 (b), ERK (c), JNK (d), IKK (e) and p65 (f) in microglia. Data are presented as mean ± SEM from four independent experiments, ***p < 0.001 versus corresponding control; #p < 0.05, ##p < 0.01 versus LPS+INF-γ-treated negative control (NC) groups. g–l Kir6.1 overexpression inhibited the phosphorylation of p38, IKK and p65 in microglia treated with LPS+INF-γ. Representative immunoblot (g) and quantitative analysis of the phosphorylation of p38 (h), ERK (i), JNK (j), IKK (k) and p65 (l) 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 LPS+INF-γ-treated vector groups
