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. 2022 Jun 22;28(4):827–840. doi: 10.3350/cmh.2022.0068

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Copyright © 2022 by The Korean Association for the Study of the Liver

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 6. — Auranofin inhibits lipid accumulation by increasing pNRF2. (A) Quantitative comparison of pNRF2 protein expression according to palmitic acid concentration. (B) pNRF2 (green), phalloidin (red), and DAPI (blue) immunofluorescence staining of PA and auranofin-treated HepG2 cells (×630). (C) Expression of pNRF2 and ubiquitinated NRF2 protein in HepG2 cells. (D) luciferase reporter activity in NRF2/ARE luciferase reporter HepG2 cells. (E) Expression of pNRF2, HO-1, and xCT proteins in HepG2 cells treated with ML385 and auranofin. (F) Comparison of lipid accumulation following oleic acid and auranofin administration in WT and ML385-treated HepG2 cells with Nile-red O staining (×630). NRF2, nuclear erythroid 2-related factor 2; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; PA, palmitic acid; DAPI, 4’,6-diamidino-2-phenylindole; ARE, antioxidant response element; WT, wile type. ^*P<0.05. ^**P<0.01. ^***P<0.001. ^****P<0.0001.