Figure 1
Figure 1. CO inhibits hepcidin expression by IL-6 and ER-stress inducers. HepG2 cells were treated with IL-6 (10 ng/mL; A), TM (10 mg/mL; B), thapsigargin (TG; 10mM; C), or homocysteine (HCYS; 1mM; D) for the indicated periods of time. The expression levels of hepcidin were analyzed by Western blotting (top panels). Cells were preincubated for 3 hours with CORM-2 (20μM) and were then exposed for 18 hours to IL-6, TM, TG, or HCYS (bottom panels). (E) HepG2 cells were treated with CORM-2 or RuCl2 and treated with TM for 18 hours. (A-E) β-actin served as the standard. Values are means ± SEM from 3 independent experiments. *P < .05; **P < .01; ***P < .001.

CO inhibits hepcidin expression by IL-6 and ER-stress inducers. HepG2 cells were treated with IL-6 (10 ng/mL; A), TM (10 mg/mL; B), thapsigargin (TG; 10mM; C), or homocysteine (HCYS; 1mM; D) for the indicated periods of time. The expression levels of hepcidin were analyzed by Western blotting (top panels). Cells were preincubated for 3 hours with CORM-2 (20μM) and were then exposed for 18 hours to IL-6, TM, TG, or HCYS (bottom panels). (E) HepG2 cells were treated with CORM-2 or RuCl2 and treated with TM for 18 hours. (A-E) β-actin served as the standard. Values are means ± SEM from 3 independent experiments. *P < .05; **P < .01; ***P < .001.

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