Table 2.
Signaling pathways | Composition structure | Signal molecules | Activation paths | Clinical effects |
---|---|---|---|---|
NF-κB | NF-κB1, NF-κB2, NF-κB3, et al. | IL-6, iNOS, ICAM1, MMP-9, COX-2, et al. | Enhances M1 activation, attenuates M2 response | Inhibits inflammatory response and increases neuroprotection |
JAK – STAT | JAKs and STAT1–6 | INF-γ, LPS, IL-10, IL-4 | Selectively activate M1 and M2 | Reduce the release of inflammatory factors and accelerate the repair of damaged nerves |
Notch | Four Notch receptors (Notch 1–4) and five Notch ligands (Delta type 1, 3, 4, sawtooth 1, 2) | unknow | Inhibit transition for M1–M2 | Promote the release of inflammatory transmitters and aggravate nerve tissue damage |
TLRs | a C-terminal TIR domain, a transmembrane region and an extracellular N-terminal | Pathogen-associated moleculars | Activation signaling pathways of NF-κB and MAPK | Increases pro-inflammatory factors and aggravates nerve damage |
IL, interleukin; ICAM1, intercellular cell adhesion molecule-1; MMP-9, Matrix Metalloproteinase 9; COX-2, Cyclooxygenase-2; INF-γ, Interferon-γ; LPS, Lipopolysaccharide; MAPK, Mitogen-activated protein kinase.