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. 2015 Jun 18;21(1):526–535. doi: 10.2119/molmed.2015.00148

Figure 6.

Figure 6

Schematic representation of SA’s mechanisms of suppression of HMGB1’s proinflammatory activities. Extracellular HMGB1 is recognized by two different receptors, CXCR4 and TLR4 (16). The fully reduced HMGB1 induces CXCR4-mediated cell migration. SA inhibits cell migration induced by HMGB1. The disulfide HMGB1 induces TLR4-mediated activation of the NF-κB signaling pathway (16,17), resulting in transcriptional activation of genes coding for COX-2 (PTGS2) and proinflammatory cytokines (IL6 and TNF ). SA suppresses disulfide HMGB1-induced PTGS2, IL6 and TNF expression.