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. 2023 Sep 18;8:355. doi: 10.1038/s41392-023-01578-2

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© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 6 — Rox treatment inhibits iron accumulation by reducing hepcidin expression and knockdown of FPN1 induces susceptibility of Mor-CPP. a PC12 cells were treated with 20 μmol/L roxadustat for 24 h. Then, the cells were prepared for ICP-MS detection of total iron content. Rox treatment lowered iron content in PC12 cells (0 μmol/L, n = 4, 20 μmol/L, n = 3, t = 4.382, df = 5, P = 0.0071). b WT mice were sacrificed after 6 h roxadustat (10 mg/kg) injection, the brain tissues, liver and serum were collected for ICP-MS detection of total iron content. Rox injection lowered iron content in STR (n = 4), PFC (n = 4) and HIP (Veh, n = 3, Rox, n = 4, drug, F_(1,17) = 21.65, P = 0.0002; area, F_(2,17) = 9.455, P = 0.0017; drug × area, F_(2,17) = 0.0007598, P = 0.9992). c, d PC12 cells were treated with 20 μmol/L Rox for 24 h. Then, the cells were prepared for q-PCR and Elisa assays, Rox treatment lowered the expression of hepcidin in PC12 cells (c, n = 6, F_(3,20) = 17.53, P < 0.0001. d, n = 7, t = 2.310, df = 12, P = 0.0395). e-i ELISA of hepcidin protein in Rox (10 mg/kg, 6 h) treated WT mice. Rox treatment lowered the expression of hepcidin in mouse liver (n = 4, t = 2.648, df = 6, P = 0.0381), serum (n = 6, t = 2.312, df = 10, P = 0.0433), STR (n = 5, t = 2.868, df = 8, P = 0.0209), PFC (n = 5, t = 3.169, df = 8, P = 0.0132), and HIP (n = 5, t = 2.807, df = 8, P = 0.0229). j The paradigm of Mor-CPP in AAV-infection mice. pAKD-CMV-bGlobin-mCherry-3*FLAG-WPRE-H1-shRNA and pAAV-CBG-mCherry-3*FLAG-WPRE-H1-shFPN1 virus were injected into NAc for 21 days before CPP performance. k, l After 21 days virus infection, mice brain tissues were collected and prepared for iron content detection with ICP-MS, FPN1 knockdown induced iron accumulation in NAc (n = 6, t = 2.294, df = 10, P = 0.0447). FPN1 knockdown mice were more sensitive to Mor-CPP as evidenced by higher CPP scores in shFPN1+Mor group as compared with Veh+Mor group. (NC-Sal, n = 13; NC-Mor, n = 12; sh-FPN1+Sal, n = 13; sh-FPN1+Mor, n = 12; group; F_(1,46) = 10.96, P = 0.0018, drug, F_(1,46) = 32.08, P < 0.0001; group × drug, F_(1,46) = 1.313, P = 0.2578). Values are presented as means ± SEM. Statistical analyses for a and d–i and k, and for b and l, and for c were performed using Student’s t-test and two-way ANOVA and one-way ANOVA followed by Bonferroni-corrected tests, respectively. *P < 0.05, **P < 0.01, ***P < 0.001