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. 2024 May 9;14(1):27. doi: 10.1007/s13659-024-00451-1

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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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Fig. 2 — Potential mechanistic pathways of the antioxidant effect of β-sitosterol leading to cardioprotective benefits using in vitro and ex vivo experiments. Mitochondrial ROS generation was enhanced by β-sitosterol. This phytosterol also increased mitochondrial respiration in states 3 and 4, decreasing coupling efficiency. In H9c2 cells, β-sitosterol increased glutathione redox cycling (GR, GSH, and GSSG) and protected against hypoxia/reoxygenation-induced apoptosis. Ex vivo, β-sitosterol protected the myocardium against I/R injury in female rats. The cardioprotective effect of β-sitosterol in this category was most likely mediated by an increase in mitochondrial glutathione redox cycling (GR, GSH, and GSSG). GR: glutathione reductase; GSH: reduced glutathione; GSSG: oxidized glutathione; ROS: reactive oxygen species; I/R: ischemia/reperfusion