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. 2024 Dec 28;14:30681. doi: 10.1038/s41598-024-76717-y

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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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Fig. 4 — CUS promotes mGCs oxidative stress and mitochondrial membrane potential change and triggers apoptosis. (A) Level of ROS, MDA, ATP measured by ELISA in ovary tissues (n = 7). (B) SOD, T-AOC measured by ELISA in ovary tissues (n = 7). (C) ROS fluorescence detection between mGCs from CUS group and Control group. (D) mGCs from CUS group find apoptosis body by TEM. (E) Detection of apoptosis in mGCs by flow cytometry (n = 3). (F) Protein expression analysis of BAX and BCL-2 in the ovaries. (G) JC-1 specifically detected mitochondrial membrane potential excitation at 405 nm fluorescence detection. (H) Mitochondrial membrane potential specifically detected with JC-1 in mGCs by flow cytometry (n = 3). *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001.