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. 2019 Jun 18;8(3):447–473. doi: 10.1016/j.jcmgh.2019.06.003

Figure 1.

Figure 1

BAR501 counteracts in vitro NKT immune activation. (A) Quantitative real-time PCR analysis of GPBAR1 expression in HepG2 (hepatocytes cell line), RAW264.7 (macrophages cell line), DN32.D3 (NKT cell line) and total spleen of GPBAR1+/+ and GPBAR1–/– mice. The data are normalized to glyceraldehyde-3-phosphate dehydrogenase (phosphorylating) (GAPDH) mRNA. Data are the mean ± SEM of 3 experiments. (B) Western blot analysis for GPBAR1 expression from the cell lysates isolated from HepG2, Raw364.7 and DN32.D3 cells. Tubulin was used as the loading control. (C) Immunohistochemistry of DN32.D3 cells with anti-GPBAR1 antibody in green. (D–G) DN32.D3 cells were incubated for 16 hours with Con A and BAR501. Quantitative real-time PCR analysis of (D) proinflammatory genes IFN-γ, IL-4, IL-17, TNF-α, and IL-2, anti-inflammatory gene IL-10, adhesion molecules CXCR6 and LFA-1, FasL, and (E) GPBAR1. (F) Analysis of cell viability through MTS assay kit. (G) ChIP assay of the CREB binding on IL-10 promoter in DN32.D3 cells. The data are normalized to GAPDH mRNA. Results are the mean ± SEM of 3 experiments. *P < .05.