Fig. 4.

Effects of Rg3-RGE with the overexpression and silencing of RXRα. For overexpression studies, various concentrations of the RXRα plasmid were transfected into RAW 264.7 cells, and the cells were then treated with Rg3-RGE. (A) Overexpression of the RXRα plasmid by real-time and RT-PCR. (B) RXRα agonist. (C) PPARγ and LXR-β agonists. (D) Nitric oxide (NO) production in RAW 264.7 cells transfected with negative control siRNA (siNCRNA), siRXRα, siPPARγ, and siLXRβ and treated with the agonists of the three nuclear receptors along with Rg3-RGE. (E) NO production was measured in RAW 264.7 cells transfected with negative control siRNA (siNCRNA), siRXRα, siPPARγ, and siLXRβ and treated with antagonists for the three receptors with Rg3-RGE. (F) Validation of siRXRα by real-time and RT-PCR. Values in the bar graph are means ± SD of three independent experiments. ***p < 0.001 was considered significant compared to the LPS-only group and where otherwise indicated. GAPDH, glyceraldehyde 3-phosphate dehydrogenase; LXRβ, liver X receptor beta; PPARγ, peroxisome-proliferating receptor γ; Rg3-RGE, Rg3-enriched red ginseng extract; RT-PCR, quantitative reverse transcription polymerase chain reaction; RXRα, retinoid X receptor α.