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. 2018 Jul 17;43(3):442–451. doi: 10.1016/j.jgr.2018.06.005

Fig. 2.

Fig. 2

Inhibition of nitric oxide (NO) production by RXRα, PPARγ, and LXRβ agonists and antagonists. RAW 264.7 cells were preincubated with Rg3-RGE, RXRα, and PPARγ agonists and antagonists for 30 minutes and then stimulated with LPS for 18 hours. Cell supernatants were then mixed with equal amounts of Griess reagent, and NO production was measured. (A) RXRα agonist (CD3594). (B) RXRα antagonist (HX531). (C) PPARγ agonist (rosiglitazone). (D) PPARγ antagonist (GW9662). (E) LXRβ agonist (GW3965). Values in the bar graph are means ± SD of three independent experiments. ***p < 0.001 was considered significant compared to the LPS-only group.LXRβ, liver X receptor beta; PPARγ, peroxisome-proliferating receptor γ; RXRα, retinoid X receptor α.