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. 2018 Feb 23;41(5):2619–2628. doi: 10.3892/ijmm.2018.3511

Figure 6.

Figure 6

DFMG inhibits the TLR4/MyD88/NF-κB pathway in LPC-injured HUVE-12 cells co-cultured with MPs, and inhibits the production of IL-1β in the co-culture supernatant. (A) Representative western blots of protein expression of TLR4, MyD88 and NF-κB p65 in LPC-injured HUVE-12 cells co-cultured with MPs. Densitometric analysis and ELISA were used to quantify the expression levels of (B) TLR4, (C) MyD88, (D) NF-κB p65 and the (E) concentration of IL-1β in the co-culture supernatant. CLI-095 and IL-1Ra downregulated the expression of these proteins and reduced the generation of IL-1β, which was promoted by co-treatment with DFMG. The data are presented as the mean ± standard deviation of three separate experiments. *P<0.05, vs. Con (without DFMG pretreatment), #P<0.05, vs. adjacent group. LPC, lysophosphatidylcholine; DFMG, 7-difluoromethoxy-5,4′-dimethoxy-genistein; MPs, macrophages; TLR4, Toll-like receptor 4; MyD88, myeloid differentiation factor 88; NF-κB, nuclear factor-κB; IL-1Ra, interleukin-1 receptor antagonist.