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. 2020 Oct 28;11(10):929. doi: 10.1038/s41419-020-03135-z

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© The Author(s) 2020

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. 7 — The rats were divided into seven groups: Sham group, I/R model group, I/R + nc-antagomir group (I/R + inc), I/R + miR-182-5p antagomir group (I/R + i-miR-182-5p), I/R + miR-378a-3p antagomir group (I/R + i-miR-378a-3p), I/R + saline group (I/R + saline), and I/R + Ferostatin-1 group (I/R + Fer-1), with 10 rats in each group. Antagomir was administrated by tail injection at the dosage of 80 mg/kg and Fer-1 was served as the ferroptosis inhibitor in AKI model by intraperitoneal injection at the concentration of 5 mg/kg. A Serum creatinine and B blood urea nitrogen levels were significantly decreased in the antagomir and Fer-1 administrated group than in the I/R group. C Iron level and D ROS level decreased in the antagomir and Fer-1 administrated group than in the I/R group. E H&E and TUNEL assay showed reduced renal tubule injury in the antagomir and Fer-1 administrated group than in the I/R group. n = 10. Data are presented as the mean ± s.e.m. **P < 0.01, ***P < 0.001 vs. indicated group.