Fig. 2: Kir6.1 deficiency facilitated the switch of microglia phenotypes from M2 to M1 in MPTP Parkinson’s disease model mice.
From: Kir6.1/K-ATP channel modulates microglia phenotypes: implication in Parkinson’s disease
a–h Kir6.1 deficiency increased the production of IL-1β (a), TNF−α (b), iNOS (c), and CCL3 (d), and reduced the expression of Arginase1 (e), CD206 (f), YM-1 (g) and TGF-β (h) in the substantia nigra compacta (SNc). i–l Kir6.1 deficiency enhanced the activation of p38 and NF-κB in the SNc. Representative immunoblot (i) and quantitative analysis of the phosphorylation of p38 (j), IKK (k) and p65 (l) in the SNc of Kir6.1+/+ and Kir6.1+/− mice. Data are presented as mean ± SEM, *p < 0.05, **p < 0.01, ***p < 0.001 versus corresponding control (saline) group; #p < 0.05, ##p < 0.01 versus MPTP-treated Kir6.1+/+ groups. n = 5 for each group. MPTP 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine
