Fig. 1

The multi-tyrosine kinase inhibitor nilotinib suppresses LPS-mediated proinflammatory responses and increases anti-inflammatory responses in BV2 microglial cells. a Structure of nilotinib. b Impact of nilotinib or vehicle on cell viability as assessed by the MTT assay (n = 14/group). c, d Immunocytochemistry of c-Abl expression in LPS-treated BV2 microglial cells pre-treated with nilotinib as shown (C: n = 54; L: n = 141; Nil + L: n = 73). e, f Immunocytochemistry of c-Abl expression in LPS-treated BV2 microglial cells post-treated with nilotinib as shown (C: n = 160; L: n = 130; L + Nil: n = 95). g Real-time PCR analysis of proinflammatory cytokine expression in LPS-treated BV2 microglial cells pre-treated with nilotinib as shown (n = 8/group). h Real-time PCR analysis of proinflammatory cytokine expression in LPS-treated BV2 microglial cells post-treated with nilotinib as shown (n = 6/group). i Real-time PCR analysis of anti-inflammatory cytokine expression in LPS-treated BV2 microglial cells post-treated with nilotinib as shown (n = 5–8/group). C: control, L: LPS, Nil + L: nilotinib + LPS, L + Nil: LPS + nilotinib, *p < 0.05, **p < 0.01, ***p < 0.001, scale bar = 20 μm