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. 2024 Jul 27;14:17318. doi: 10.1038/s41598-024-67557-x

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© The Author(s) 2024

Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, 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 you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. 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-nc-nd/4.0/.

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Knockdown of Nrf2 reverses the protective effect of ICA on cis-induced KGN cell injury. (A) and (B), KGN cells were transfected with Nrf2 siRNA or negative control (NC) siRNA, and the protein levels of Nrf2, HO-1, Gpx4, γH2AX, and Bax were assessed by WB (A) and quantified (B). (C) and (D), Detection of cell viability and cytotoxicity of KGN cells in different treatment groups using CCK8 (C) and LDH (D), respectively. (E,F) , ROS were detected using DCFH-DA (E) and quantified (F). (G) and (H), Lipid peroxidation levels were detected using C11-BODIPY 581/591 probes (G) and quantified (H). (I) and (J), The percentage of apoptosis of KGN cells in different treatment groups was detected using Annexin V/PI staining and flow cytometry. Data are presented as mean ± SEM, *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001, ns, non-statistically significant.