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. 2021 Nov 30;4(6):1835–1848. doi: 10.1021/acsptsci.1c00224

Figure 1.

Figure 1

Lodoxamide suppresses LXR-mediated accumulation of lipid in HepG2 cells: This is potentially a GPR35-mediated effect. HepG2 cells (scale bar = 100 μm) were treated for 48 h with the LXR activator T0901317 (4 × 10–6 M) or with T0901317 and various concentrations of lodoxamide (1 × 10–8–1 × 10–5 M). Subsequently, cells were stained with Oil Red O and visualized (lodoxamide = 1 × 10–5 M) (A) or lipid-fixed Oil Red O was solubilized and quantified by measuring absorbance at 510 nm (B). The effect of varying concentrations of lodoxamide is shown (C). Data are presented as representative images (A) or mean ± SEM, n = 3 (B, C). (D) RT-PCR studies identified expression of the human GPR35b slice variant but not GPR35a by HepG2 cells and HT-29 cells, while THP-1 monocyte-like cells expressed GPR35a. Anticipated base pair (bp) sizes, GPR35a, 737 bp; GPR35b, 464 bp. mRNA levels of GPR35b in HepG2 cells were unaffected by treatment with T0901317 with or without lodoxamide. Human (h)GAPDH provided an internal control. Co-addition of the human GPR35 antagonists CID-2745687 (E) or ML-145 (F) prevented the effect of lodoxamide on lipid accumulation (p < 0.05, a: versus vehicle, b: versus T0901317, and c: versus T0901317/lodoxamide).