Fig. 2
Molecular mechanisms of activation of α7 nAChR-mediated CAP. The activation of α7 nAChR could inhibit the expression of NF-κB through TLR4/NF-κB/NLRP3, JAK2/STAT3/NF-κB and Ca2+-related signaling pathways, reduce the production of inflammatory cytokines, reduce neuroinflammation, and finally play an antidepressant role. ↑: upregulate, ↓: downregulate, TLR4 Toll-like receptors 4, MyD88 myeloid differentiation factor 88, IKK inhibitor of kappa B kinase, IκB inhibitor of NF-κB, JAK2 Janus Kinase 2, STAT3 signal transduction and transcription activator 3, SOCS3 suppressor of cytokine signaling 3, NF-κB nuclear factors-kappa B, PLC phospholipase C, IP3 inositol 1,4,5-triphosphate, PI3K phosphatidylinositol 3-kinase, Akt protein kinase B, GSK-3 glycogen synthase kinase 3, BDNF brain-derived neurotrophic factor, TrkB tropomyosin receptor kinase B, ERK extracellular signal-regulated kinase, CaMKII Ca2+/calmodulin-dependent protein kinase II, CaMKIV Ca2+/calmodulin-dependent protein kinase IV, JNK c-Jun N-terminal kinase, Nrf2 nuclear transcription factor E2-related factor, HO-1 heme oxygenase-1, ROS reactive oxygen species, CREB cAMP-response element binding protein, NLRP3 NOD-like receptor protein 3, IL-1β interleukin-1β, IL-6 interleukin-6, TNF-α tumor necrosis factor-α, NO nitric oxide