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. 2018 Jun 15;32(12):6724–6736. doi: 10.1096/fj.201701381

Figure 5.

Figure 5

Effect of LXR activation on cigarette smoke–induced acute pulmonary inflammation and MMP activation. Total inflammatory cell counts in BAL fluid (BALF) of mice exposed to cigarette smoke for 10 d with or without LXR agonist treatment vs. room air–exposed control mice (n = 4). A) Protein concentration of TNF-α. B) mRNA analysis of ABCA1, MMP-9, and TNF-α in BAL cells of mice exposed to cigarette smoke for 10 d with or without LXR agonist treatment vs. room air–exposed control mice. C) mRNA analysis of ABCA1, MMP-9, and TNF-α in the lungs of mice exposed to cigarette smoke for 10 d with or without LXR agonist treatment vs. room air–exposed control mice. D) Protein concentrations of IL-1β, IL-6, IL-17, IFN-γ, monocyte chemoattractant protein 1 MCP-1, and TNF-α measured by Luminex cytokines array system in the lungs of mice exposed to cigarette smoke for 10 d with or without LXR agonist treatment vs. room air–exposed control mice. E) β-Actin was used as a housekeeping gene control for real-time PCR. *P < 0.05, **P < 0.01, ***P < 0.001 when compared with controls, #P < 0.05 compared with 10 d of cigarette smoke exposure (significantly significant).