Fig. 2

Nilotinib suppresses LPS-stimulated AKT/P38/STAT3 signaling in BV2 microglial cells. a, b RT-PCR analysis of proinflammatory cytokine IL-1β expression in BV2 microglial cells treated sequentially with LPS, TLR4 inhibitor (TAK-242) and nilotinib as shown (n = 7/group). c Real-time PCR analysis of proinflammatory cytokine COX-2 mRNA expression in BV2 microglial cells treated sequentially with LPS, TLR4 inhibitor (TAK-242) and nilotinib as shown (n = 8/group). d, e Western blotting analysis of AKT/P38 signaling in LPS-treated BV2 microglial cells post-treated with nilotinib as shown (n = 5/group). f–i Immunocytochemistry analysis of AKT/P38 signaling in LPS-treated BV2 microglial cells post-treated with nilotinib (p-AKT, C: n = 181; L: n = 162; L + Nil: n = 111, p-P38, C: n = 197; L: n = 246; L + Nil: n = 157). j Western blot analysis of nuclear p-STAT3 expression in LPS-treated BV2 microglial post-treated with nilotinib as shown (n = 4/group). k Immunocytochemistry analysis of p-STAT3 levels in LPS-treated BV2 microglial cells post-treated with nilotinib as shown in j (C: n = 110; L: n = 161; L + Nil: n = 94). C: control, L: LPS, Nil + L: nilotinib + LPS, *p < 0.05, **p < 0.01, ***p < 0.001, scale bar = 20 μm