Figure 7.

Schematic diagram of the targets for DMOG. LPS promoted the activation of PI3K/AKT, NF‐κB and MAPK signalling pathway via TLR4/MyD88‐dependent manner to upregulate proinflammatory cytokine expression. Our study demonstrated that DMOG inhibited LPS‐upregulated TLR4 and MyD88 expression and subsequently suppressed the phosphorylation and degradation of IκBα. Afterwards, the phosphorylation and nuclear translocation of NF‐κB p65 were reduced. Moreover, DMOG inhibited AKT phosphorylation, which might interact with IKKs, the upstream kinase of NF‐κB. Likewise, the activation of MAPK which was also implicated in LPS‐induced inflammation was downregulated by DMOG. Consequently, LPS‐upregulated inflammatory cytokine expression was attenuated. LPS, lipopolysaccharide; TLR4, Toll‐like receptor 4; MyD88, myeloid differentiation primary response protein 88; DMOG, dimethyloxallyl glycine; IκBs, inhibitors of NF‐κB; PI3K, phosphoinositide‐3‐kinase; AKT/ PKB, protein kinase B; NF‐κB, nuclear factor kappa B; MAPK, mitogen‐activated protein kinase; JNK, c‐Jun N‐terminal kinase; ERK, extracellular signal regulated kinase; AP‐1, Activator protein 1