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Formononetin (FMN), which is a major bioactive isoflavone compound in <jats:italic>Astragalus membranaceus<\/jats:italic>, exerts anti-inflammatory effects. However, whether FMN is effective in the treatment of PCOS remains unknown. This study aims to explore the effects and the possible mechanisms of FMN in PCOS.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Methods<\/jats:title>\n            <jats:p>Dehydroepiandrosterone (DHEA)-induced PCOS rats and dihydrotestosterone (DHT)-induced PCOS cell models were established. Fifty rats were randomly assigned into five groups of 10 rats each: Control, PCOS, PCOS\u2009+\u2009FMN (15\u00a0mg\/kg), PCOS\u2009+\u2009FMN (30\u00a0mg\/kg), and PCOS\u2009+\u2009FMN (60\u00a0mg\/kg). Fasting blood glucose, insulin, luteinizing hormone, follicle-stimulating hormone, testosterone, and estradiol were detected in DHEA-induced PCOS rats. Ovarian histological changes and apoptosis were evaluated utilizing H&amp;E and TUNEL staining. Subsequently, the effects of FMN on oxidative stress and inflammatory responses in the DHEA-induced PCOS rat model and DHT-induced PCOS cell model were explored. Besides, the function of FMN on cell viability and apoptosis in DHT-induced PCOS cell model were explored by using CCK-8 assay and flow cytometry. Protein expression was detected via western blot and immunofluorescence staining in the DHEA-induced PCOS rat model and DHT-induced PCOS cell model.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Results<\/jats:title>\n            <jats:p>FMN alleviated PCOS symptoms and reduced inflammation, cell apoptosis, and oxidative stress in DHEA-induced PCOS rats and DHT-induced KGN cells. Additionally, FMN suppressed NLRP3 inflammasome activation in both models. In the DHT-induced PCOS cell model, nigericin (a activator of NLRP3) reversed the functions of FMN on inflammation, apoptosis, and oxidative stress.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusion<\/jats:title>\n            <jats:p>These findings demonstrated that FMN could alleviate PCOS by repressing inflammation, apoptosis, as well as oxidative stress in vivo and in vitro via inhibition of the NLRP3 inflammasome.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Highlights<\/jats:title>\n            <jats:p>\n              <jats:list list-type=\"order\">\n                <jats:list-item>\n                  <jats:p>FMN improved PCOS symptoms.<\/jats:p>\n                <\/jats:list-item>\n                <jats:list-item>\n                  <jats:p>FMN alleviated cell apoptosis, inflammation and oxidative stress in PCOS.<\/jats:p>\n                <\/jats:list-item>\n                <jats:list-item>\n                  <jats:p>FMN inhibited the activation of NLRP3 inflammasome in PCOS.<\/jats:p>\n                <\/jats:list-item>\n              <\/jats:list>\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1186\/s10020-025-01092-x","type":"journal-article","created":{"date-parts":[[2025,1,27]],"date-time":"2025-01-27T09:17:38Z","timestamp":1737969458000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":31,"title":["Formononetin ameliorates polycystic ovary syndrome through suppressing NLRP3 inflammasome"],"prefix":"10.1186","volume":"31","author":[{"given":"Zhuo","family":"Liu","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rui-Han","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ke-Hua","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2025,1,27]]},"reference":[{"issue":"4","key":"1092_CR1","doi-asserted-by":"publisher","first-page":"1243","DOI":"10.1093\/advances\/nmab141","volume":"13","author":"S Alesi","year":"2022","unstructured":"Alesi S, Ee C, Moran LJ, Rao V, Mousa A. 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