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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. 5 — Effect of CUS on glycolysis level and mitochondrial function in mGCs. (A) The mGCs analyze extracellular acidification rate (ECAR) by Seahorse Glycolytic Rate Assay (Glucose:10mM Glucose, Oligomycin: electron transport chain(ETC) complex IV inhibitors, 2-DG: 2-deoxy-glucose, hexokinase competitive inhibitors ). (B–D) Non-glycolytic acidification, glycolysis and glycolytic capacity in seahorse glycolytic stress test assay; (E) The mGCs analyze oxygen consumption rate (OCR) by seahorse Mito stress assay (FCCP: Carbonyl cyanide-4 (trifluoromethoxy)Phenylhydrazone, Mitochondrial uncouplers that completely disrupt proton gradients and mitochondrial membrane potential, Rotenone: ETC complex I inhibitors, Antimycin A: ETC complex III inhibitors). (F–H) Basal respiration, maximal respiration and ATP production in seahorse Mito stress assay. ns, no significance; *, P < 0.05; **, P < 0.01.