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. Author manuscript; available in PMC: 2014 Jan 6.
Published in final edited form as: Nutr Rev. 2011 Jun;69(6):10.1111/j.1753-4887.2011.00394.x. doi: 10.1111/j.1753-4887.2011.00394.x

Fig.1. Identified molecular targets of phytochemicals on PRR-mediated inflammatory signaling pathway.

Fig.1

TLRs and NODs are pathogen recognition receptors (PRRs) that detect conserved molecules of pathogens. Stimulation of TLRs by ligands leads to the recruitment of adaptor molecules such as MyD88 and TRIF through the interaction of TIR domains, leading to MyD88 dependent and MyD88-independent (TRIF dependent) signaling pathway. The activation of NODs leads to the recruitment of RICK/RIP2 through CARD–CARD interactions, leading to activation of inflammatory signaling pathway. Curcumin, helenalin, cinnamaldehyde, and sulforaphane inhibit TLR4-mediated NF-κB activation by inhibiting TLR4 dimerization. Resveratrol, EGCG, luteolin, quercetin, chrysin, and eriodictyol directly inhibit TBK1 kinase activity. Similarly, curcumin, helenalin and parthenolide also inhibit NOD2 mediated NF-κB activation, presumably through inhibition of NOD2 dimerization.