{"paper_id":"ce065c80-b40a-48b5-980a-1f3eae446682","body_text":"Abstract\nObjective\nThe aim of this study was to investigate the role and mechanism of Sulforaphane (SFN) in ameliorating endometriosis (EMs).\nMethods\nEMs’ rat model was established by autotransplantation method and administered with low, medium, and high doses of SFN. The volume and weight of the lesions were measured, the histopathological changes of the endometrium were observed by HE staining, and autophagy proteins were detected by immunofluorescence staining, whereas VEGF and apoptosis-related proteins were detected by Western blot. Rat primary endometrial stromal cells (ESCs) were isolated. Cell viability was determined by MTT, apoptosis by Tunel, migration and invasion by Transwell, and apoptotic and autophagic proteins by Western blot. Mitochondrial membrane potential, ATP content, and ROS levels were assessed for cellular mitochondrial function. Chloroquine (CQ), an autophagic flux inhibitor (AFI), was used alone or in combination with SFN to intervene cells.\nResults\nSFN inhibited the growth of EMs rat lesions in a dose-dependent pattern, alleviated the pathological changes of endometrium, downregulated VEGF, and upregulated apoptosis in endometrial tissues. Different concentrations of SFN effectively inhibited cell viability, migration, and invasion, and promoted apoptosis in rat ESCs, and the effects were concentration-dependent. SFN regulated autophagy proteins and inhibited autophagic flux. SFN disrupted the mitochondrial function of ESCs. CQ intervention alone inhibited ESCs cell viability, migration, and invasion, promoted apoptosis, and disrupted cellular mitochondrial function. Combined CQ intervention had a synergistic effect on SFN in regulating the biological phenotype and mitochondrial function of ESCs.\nConclusion\nSFN ameliorates EMs in rats by modulating autophagy and mitochondrial dysfunction.\nSimilar content being viewed by others\nAvailability of data and materials\nThe datasets used and/or analyzed during the present study are available from the corresponding author on reasonable request.\nReferences\nAllaire C, Bedaiwy MA, Yong PJ (2023) Diagnosis and management of endometriosis. CMAJ 195(10):E363–E371\nAllavena G, Carrarelli P, Del Bello B, Luisi S, Petraglia F, Maellaro E (2015) Autophagy is upregulated in ovarian endometriosis: a possible interplay with p53 and heme oxygenase-1. Fertil Steril 103(5):1244–51.e1\nAparicio R, Hansen M, Walker DW, Kumsta C (2020) The selective autophagy receptor SQSTM1/p62 improves lifespan and proteostasis in an evolutionarily conserved manner. 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All authors contributed to editorial changes in the manuscript. All authors read and approved the final manuscript.\nCorresponding author\nEthics declarations\nCompeting interests\nDongMei Pang, MouChang Qiu and FeiFei Xu declare that they have no conflict of interest.\nEthical statement\nAll animal experiments were complied with the ARRIVE guidelines and performed in accordance with the National Institutes of Health Guide for the Care and Use of Laboratory Animals. The experiments were approved by the Institutional Animal Care and Use Committee of The Affiliated Taizhou People’s Hospital of Nanjing Medical University.\nAdditional information\nPublisher's Note\nSpringer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.\nSupplementary Information\nBelow is the link to the electronic supplementary material.\nRights and permissions\nSpringer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.\nAbout this article\nCite this article\nPang, D., Qiu, M. & Xu, F. Sulforaphane ameliorates endometriosis in rats by modulating autophagy and mitochondrial dysfunction. Mol. Cell. Toxicol. (2025). https://doi.org/10.1007/s13273-025-00570-x\nReceived:\nRevised:\nAccepted:\nPublished:\nVersion of record:\nDOI: https://doi.org/10.1007/s13273-025-00570-x","source_license":"CC0","license_restricted":false}