fig2

Figure 2. Mediators of microglial polarization after SAH. Activation of TLR4, HMGB1, STAT3 and MAPK signaling pathways promotes microglial M1 polarization with the expression of TNF-α, IL-1β, IL-6 and ICAM-1. The downstream mediators are shown in the figure. Activation of TSG-6 and mGluR5 promotes microglial M2 polarization, therefore reverses the pro-inflammatory responses. SAH: subarachnoid hemorrhage; TLR4: toll-like receptor 4; HMGB1: high-mobility group box 1 protein; STAT3: signal transducer and activator of transcription 3; MAPK: mitogen-activated protein kinase; TNF-α: tumor necrosis factor-α; IL: interleukin; ICAM-1: intercellular adhesion molecule 1; TSG-6: tumor-specific glycoprotein-6; mGluR5: metabotropic glutamate receptor 5; JAK2: Janus kinases 2; MyD88: myeloid differentiation factor 88; SOCS3: suppressor of cytokine signaling 3; TGF-β: transforming growth factor-β; NF-kB: nuclear factor kappa-light-chain-enhancer of activated B cells; Prx2: peroxiredoxin 2; metHgb: methemoglobin