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. 2018 Oct 11;59(12):2287–2296. doi: 10.1194/jlr.M084558

Fig. 5.

Fig. 5.

Inhibition of HSV-1 infection by LXR activation is correlated to induction of CH25H expression in a cell type-dependent manner. A, B: Comparison of basal levels of CH25H and IFN-γ protein (A, upper panel) and induction of CH25H and LXR protein expression by T317 treatment for 16 h (B) between RAW 264.7 macrophages and HepG2 cells. Induction of macrophage IFN-γ expression by 25HC (A, lower panel): RAW 264.7 cells were treated with 25HC at the indicated concentrations overnight. C: RAW 264.7 macrophages were pretreated with T317 for 24 h and then infected with HSV-1 (MOI = 0.05) for 2 h and continued T317 treatment in fresh complete medium for 16 h. D, E: HepG2 and RAW 264.7 cells were treated with T317 or 25HC for 24 h and then infected with HSV-1 infection (MOI = 0.05) for 2 h and continued T317 or 25HC treatment for 16 h. Expression of CH25H, IFN-γ, LXRα, and LXRβ (A, B) and HSV-1 infection (C–E) in RAW 264.7 macrophages and HepG2 cells were determined by Western blot, respectively. aP < 0.05, bP < 0.01 versus control or as indicated (n = 3).