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

Figure 4.

Figure 4

DFMG represses activation of the TLR4/MyD88/NF-κB pathway in LPC-injured HUVE-12 cells co-cultured with MPs, and reduces the generation of IL-1β in the co-culture supernatant. (A) Representative western blots of protein expression levels of TLR4, MyD88 and NF-κB p65 in HUVE-12 cells co-cultured with MPs. Densitometric analysis was used to quantify the protein levels of (B) TLR4, (C) MyD88 and (D) NF-κB p65. DFMG (0.3, 1.0 and 3.0 µM) downregulated the expression of these proteins. (E) DFMG (1.0 and 3.0 µM) decreased the concentration of IL-1β in the co-culture supernatant. The data are presented as the mean ± standard deviation of three separate experiments. *P<0.05, vs. DMSO group, #P<0.05, vs. LPC 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-1β, interleukin-1β; DMSO, dimethyl sulfoxide; OD, optical density.