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. 2021 Oct 23;13(11):3739. doi: 10.3390/nu13113739

Figure 3.

Figure 3

Signaling and pathways in which equol exerts anti-inflammatory effects. (A): PGE2 pathway [61]. (B): TNF-α [62] and IL-1 pathway [69]. (C): TLR4 [65] and IL-6 pathway [69]. (D): MCP-1 pathway [64]. “⏊” indicates the inhibitory effect by equol. PGE2: prostaglandin E2, cAMP: cyclic adenosine monophosphate, PKA: protein kinase A, IL: interleukin, TNF: tumor necrosis factor, iNOS: nitric oxide system, TNFR: TNF receptor, TRADD: TNFR1-associated death domain protein, TRAF2: TNF receptor-associated factor 2, PI3K or Akt: phosphoinositide 3-kinases, MAPK or P38: mitogen-activated protein kinase, AP: activator protein, NF-kB: nuclear factor kappa B, ICAM: intercellular adhesion molecule, VCAM: vascular cell adhesion molecule, IL-R: interleukin receptor, LPS: lipopolysaccharide, TLR: Toll-like receptor, TRIF: Toll/IL-1R domain-containing adaptor-inducing IFN-β, TRAM: TRIF-related adaptor molecule, TRAF: TNFR-associated factor, RIP: receptor-interacting protein, IRF: IFN regulatory factor, IFN: interferon, JAK: janus kinase, SHP: Src homology-2 domain-containing protein tyrosine phosphatase, AR: androgen receptor, MCP: monocyte chemoattractant protein, CCR: Chemokine receptor, MCPIP: monocyte chemoattractant protein-induced protein.