Fig. 17

A working model for how dasatinib alters LPS-induced proinflammatory responses in BV2 microglial cells, primary microglial cells, and primary astrocytes. a In BV2 microglial cells, dasatinib treatment inhibits TLR4/ERK signaling, leading to suppression of LPS-induced nuclear p-STAT3 and/or other transcription factors and, in turn, reduced LPS-induced proinflammatory cytokine COX-2 mRNA levels. b Dasatinib treatment inhibits TLR4/AKT signaling in BV2 microglial cells, leading to suppressed LPS-induced proinflammatory cytokine IL-6 mRNA levels. c Dasatinib treatment of primary microglial cells inhibits AKT signaling and results in downregulation of LPS-induced proinflammatory cytokine levels. d In primary astrocytes, dasatinib treatment prevents AKT phosphorylation, which decreases LPS-induced nuclear p-STAT3 levels and subsequently leads to downregulation of LPS-induced proinflammatory cytokine levels