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. 2022 Feb 23;12:3056. doi: 10.1038/s41598-022-06848-7

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© The Author(s) 2022

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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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PAEC ferroptosis induces HMGB1 release, upregulates macrophage TLR4 expression and activates the NLRP3 inflammasome in vitro. (A) Bar graph showing that Fer-1 treatment significantly inhibited HMGB1 release in PAECs derived from MCT-induced rats. (B) Representative images showing the effect of Fer-1 on TLR4 expression in cocultured macrophages (NR8383 cell line). (C) Bar graph showing that Fer-1 treatment significantly restored TLR4 protein expression in cocultured macrophages. (D-J) TAK-242 significantly inhibited the increase in TLR4 and restored the upregulated expression of NLRP3 inflammasome-related proteins (ASC, NLRP3, pro-caspase1, and caspase1 and ratio of caspase1/pro-caspase1). The group of blots were cropped from the same gel. (K-M) Effects of TAK-242 on the secretion of TNF-α, IL-1β, and IL-18 in cocultured macrophages. Each experiment was repeated 3 times, n = 3. HMGB1, High-mobility group box-1 protein. *P < 0.05 versus the negative group; #P < 0.05 versus the HMGB1 group.