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. 2018 Aug 3;42(5):2551–2559. doi: 10.3892/ijmm.2018.3807

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Copyright: © Lee et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Sorafenib and UDCA trigger ROS production and activate ERK in a time- and concentration-dependent manner. (A) Huh-BAT and HepG2 cells were treated with 5 μM sorafenib, 750 μM UDCA, or both, or with 5 mM NAC for 48 h. ROS generation was measured by confocal fluorescence microscopy. Magnification, ×400. (B) Quantitative analysis of ROS generation. (C) Huh-BAT cells were treated with various doses of UDCA or sorafenib for 48 h. (D) Huh-BAT cells were treated with 750 μM UDCA or 5 μM sorafenib for various timepoints. (E) HepG2 cells were treated with various doses of UDCA or sorafenib for 48 h. (F) HepG2 cells were treated with 750 μM UDCA or 5 μM sorafenib for various timepoints. (G) Cells were treated with 5 μM sorafenib, 750 μM UDCA or both for 48 h. Protein expression levels of ERK and phospho-ERK were evaluated by western blotting. β-actin was used as a loading control. Representative blots and quantifications are shown. Data are presented as means ± standard deviation. ^*P<0.05 and ^**P<0.01 compared with control untreated cells. UDCA, ursodeoxycholic acid; ROS, reactive oxygen species; ERK, extracellular signal-regulated kinase; NAC, N-acetyl cysteine.

Sorafenib and UDCA trigger ROS production and activate ERK in a time- and concentration-dependent manner. (A) Huh-BAT and HepG2 cells were treated with 5 μM sorafenib, 750 μM UDCA, or both, or with 5 mM NAC for 48 h. ROS generation was measured by confocal fluorescence microscopy. Magnification, ×400. (B) Quantitative analysis of ROS generation. (C) Huh-BAT cells were treated with various doses of UDCA or sorafenib for 48 h. (D) Huh-BAT cells were treated with 750 μM UDCA or 5 μM sorafenib for various timepoints. (E) HepG2 cells were treated with various doses of UDCA or sorafenib for 48 h. (F) HepG2 cells were treated with 750 μM UDCA or 5 μM sorafenib for various timepoints. (G) Cells were treated with 5 μM sorafenib, 750 μM UDCA or both for 48 h. Protein expression levels of ERK and phospho-ERK were evaluated by western blotting. β-actin was used as a loading control. Representative blots and quantifications are shown. Data are presented as means ± standard deviation. ^*P<0.05 and ^**P<0.01 compared with control untreated cells. UDCA, ursodeoxycholic acid; ROS, reactive oxygen species; ERK, extracellular signal-regulated kinase; NAC, N-acetyl cysteine.