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. 2024 Feb 9;14:3335. doi: 10.1038/s41598-024-53976-3

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© The Author(s) 2024

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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Inhibition of Nrf2 aggravates LPS-induced HUVECs ferroptosis and inflammation. (A) Western blot was used to verify the inhibition effect of Nrf2 in endothelial cells by ML385(5 μM) treatment at different times (0, 6, 12, and 24 h); ***P < 0.001 versus 0 h group. (B) CCK8 was used to detect cell viability after LPS treatment for 24 h; **P < 0.01, ***P < 0.001. (C) The DCFH-DA probes were performed for ROS levels (scale bar, 200 μm) after LPS treatment for 3 h. (D) The iron ion, GSH, and MDA levels were measured after LPS treatment for 6 h; *P < 0.05, **P < 0.01, ***P < 0.001. (E) The ferroptosis-related protein expression levels were measured by western blot after LPS treatment for 6 h; *P < 0.05 versus Control group, ^#P < 0.05 versus LPS group. (F) The LPS (6 h)-induced inflammation-related proteins after ML385(5 μM) treatment were measured by western blot ; *P < 0.05 versus Control group, ^#P < 0.05 versus LPS group, ^¥P < 0.05 versus LPS + ML385 group.