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

Figure 5.

Figure 5

TLR4/MyD88/NF-κB pathway is involved in the activation of MPs induced by co-culture with LPC-injured HUVE-12 cells. (A) CLI-095 and IL-1Ra effectively reduced the cell viability of MPs co-cultured with LPC-injured HUVE-12 cells, which were enhanced by co-treatment with DFMG (magnification, ×200). (B) Graph and (C) images of wound healing assay showed that CLI-095 and IL-1Ra effectively increased the relative wound area of MPs, which were promoted by DFMG (magnification, ×100). (D) Images and (E) quantification showed that CLI-095 and IL-1Ra effectively reduced lipid accumulation in MPs co-cultured with LPC-injured HUVE-12 cells, which were enhanced by co-treatment with DFMG (magnification, ×200). The data are presented as the mean ± standard deviation of three separate experiments. *P<0.05, vs. Con (without DFMG pretreatment) group, #P<0.05, vs. adjacent group. LPC, lysophos-phatidylcholine; 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; OD, optical density.