Sulforaphane ameliorates endometriosis in rats by modulating autophagy and mitochondrial dysfunction

Danmei Pang, Mantang Qiu, MouChang Qiu, Feifei Xu
In: Molecular & Cellular Toxicology · 2025 · doi:10.1007/s13273-025-00570-x · W4414113054
article OA: closed CC0
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⚙ AI-generated summary by claude@2026-06+body, 2026-06-06 ⓘ

Sulforaphane inhibited endometriosis lesion growth in rats and rat endometrial stromal cells by promoting apoptosis, inhibiting migration and invasion, and modulating autophagy and mitochondrial dysfunction.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-06 ⓘ

The study investigated whether sulforaphane (SFN) ameliorates endometriosis in a rat model generated by autotransplantation, using dose-ranging SFN administration alongside measurements of lesion volume/weight, histopathology (HE staining), VEGF and apoptosis-related proteins (Western blot), and autophagy proteins (immunofluorescence). SFN inhibited lesion growth in a dose-dependent manner, reduced endometrial pathological changes, downregulated VEGF, and increased apoptosis in endometrial tissues and in rat endometrial stromal cells (ESCs), where it also decreased cell viability, migration, and invasion while disrupting mitochondrial function; SFN effects were concentration-dependent. Mechanistically, SFN altered autophagy-related proteins and inhibited autophagic flux, and the autophagic flux inhibitor chloroquine showed that autophagy inhibition also impaired ESC phenotypes and mitochondrial function, with combined SFN and chloroquine producing synergistic effects. The paper does not explicitly discuss limitations such as sample size, blinding/randomization, or whether findings translate to humans. This paper is centrally about endometriosis — it tests SFN treatment in rats and links its effects to autophagy modulation and mitochondrial dysfunction.

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Condition tags

endometriosis

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