Figure 3.

Activation of inflammatory signaling. Extracellular stimuli such as oxidative stress, TLRs activation, and infection lead to activating MAPK pathways by phosphorylation of ERK, JNK, and p38. Then, NF-κB is translocated to the nucleus, which in turn binds to DBD of its target genes, proinflammatory cytokines, proinflammatory enzymes, and CRP. The target genes of NF-κB are well known for aggravating inflammation responses. TLRs: toll-like receptors; ERK: extracellular signal-regulated kinases; JNK: c-Jun NH2-terminal; DBD: DNA binding domain; IL: interleukin; TNF-α: tumor necrosis factor-α; COX-2: cyclooxygeneases-2; iNOS: inducible nitric oxide synthase; LOX: lipoxygenase; CRP: C-reactive protein.