Figure 3
Figure 3. EPO inhibits LPS-mediated hepcidin induction independently of IL-6 production. (A) IL-6 mRNA levels in liver, (B) IL-6 levels in serum, and (C) intrahepatic IL-6 protein levels in mice treated with saline (CTL), EPO, LPS, and mice with combined treatments (EPO + LPS). (D) Hepcidin mRNA levels in the liver of mice treated with saline (CTL), EPO, mouse recombinant IL-6 (IL-6), and mice with combined treatments (EPO + IL-6). IL-6 and hepcidin mRNA levels were quantified by real-time RT-PCR and normalized to β-actin. The IL-6/β-actin and hepcidin/β-actin ratios are shown. IL-6 protein levels were measured by ELISA. Statistical analysis was performed by 1-way ANOVA; *P < .01 and **P < .001 for comparison with control mice. Data are presented as means plus or minus SD with n = 6 mice per group in panels A through C and as individual mice in panel D. n.s. indicates not significant.

EPO inhibits LPS-mediated hepcidin induction independently of IL-6 production. (A) IL-6 mRNA levels in liver, (B) IL-6 levels in serum, and (C) intrahepatic IL-6 protein levels in mice treated with saline (CTL), EPO, LPS, and mice with combined treatments (EPO + LPS). (D) Hepcidin mRNA levels in the liver of mice treated with saline (CTL), EPO, mouse recombinant IL-6 (IL-6), and mice with combined treatments (EPO + IL-6). IL-6 and hepcidin mRNA levels were quantified by real-time RT-PCR and normalized to β-actin. The IL-6/β-actin and hepcidin/β-actin ratios are shown. IL-6 protein levels were measured by ELISA. Statistical analysis was performed by 1-way ANOVA; *P < .01 and **P < .001 for comparison with control mice. Data are presented as means plus or minus SD with n = 6 mice per group in panels A through C and as individual mice in panel D. n.s. indicates not significant.

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