Effects of metformin and ganirelix on subcutaneous endometriosis in a mouse model of autophagy-related cell death

Gamze Sönmez Ünal, Yasemin Albak, Nazan Yurtçu, Çağlar Yıldız, Meral Çetin, Sevgi Durna Daştan, Erkan Gümüş, Ali Çetin
Turkish journal of obstetrics and gynecology · 2023 · vol. 20(3) , pp. 219–226 · doi:10.4274/tjod.galenos.2023.85616 · PMID:37667560 · W4386421758
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⚙ AI-generated summary by claude@2026-06, 2026-06-10 ⓘ

Metformin and ganirelix treatment in a mouse endometriosis model significantly decreased Beclin1, Beclin2, and LC3BII gene expression, suggesting metformin may suppress endometriosis via an autophagy-based mechanism.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-10 ⓘ

This study used a mouse model of subcutaneous endometriosis created by transplanting autologous endomyometrial tissue into the subcutaneous space, and then tested how metformin and the GnRH antagonist ganirelix—alone or in combination—affected endometriotic lesion regression and autophagy-related biomarkers (Beclin 1, Beclin 2, and LC3BII) using qRT-PCR and histopathology. Treatment was initiated either 24 hours or 7 days after lesion creation, continued through a second surgery two weeks later, and lesions were assessed for shrinkage, regression rates, epithelial/gland/stromal preservation, and inflammation, with additional immunohistochemical evaluation of Wnt2 and HIF1α. The paper’s key finding was that modulating these interventions changed autophagy marker expression alongside histopathologic lesion features, supporting an “autophagy-based suppression mechanism,” though the summary is limited by reliance on the biomarker panel and the report’s relatively small n per group (8 mice) plus the short-duration, subcutaneous model context. This paper is centrally about endometriosis — it evaluates metformin and ganirelix effects on subcutaneous endometriotic lesion regression in relation to autophagy-related cell-death pathways.

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Abstract

Objective: This study aimed to investigate the efficacy of metformin and ganirelix on subcutaneous endometriotic tissues created in an experimental mouse model. Materials and Methods: gene analyzes. Drug effects were examined by histological examination. HIF1a and WNT2 protein expressions were examined immunohistochemically. Gene expression coefficients of control, metformin day 1 (Met1g), metformin day 7 (Met7g), ganirelix day 1 (Gnx1g), and ganirelix day 7 (Gnx7g) groups are shown in tables. Data are presented as mean and standard error. Results: day groups. These findings were supported by histological and immunohistochemical staining. Conclusion: These genes are actively involved in the autophagy pathway, and we think that the use of metformin in endometriosis might create an autophagy-based suppression mechanism.

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endometriosis

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