Effect of rapamycin on endometriosis in mice

X U Ren, Xu Ren, Yifeng Wang, Gang Xu, Libing Dai
Experimental and therapeutic medicine · 2016 · vol. 12(1) , pp. 101–106 · doi:10.3892/etm.2016.3280 · PMID:27347023 · W2340786495
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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

Rapamycin treatment in mice significantly reduced endometriotic lesion volume by inhibiting vascular endothelial growth factor expression and subsequent angiogenesis.

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

This study investigated whether rapamycin (RAPA), an mTOR inhibitor, reduces endometriosis (EMS) lesion growth and angiogenesis in a human-tissue xenograft EMS-SCID mouse model, with lesion volumes measured after 2 weeks of treatment in RAPA-, saline-, and untreated control groups (n=10/group). Serum HIF-1α and VEGF were quantified by ELISA, and lesion expression of HIF-1α, VEGF, and CD34, along with microvessel density (MVD), were assessed by immunohistochemistry. RAPA significantly reduced EMS lesion volume, and was associated with lower serum and lesion VEGF levels and reduced MVD, while HIF-1α effects were not highlighted as differing between groups; the paper does not explicitly state limitations such as sample size or lack of additional mechanistic assays. This paper is centrally about endometriosis — it tests rapamycin’s effects on endometriotic lesion growth and angiogenesis in mice.

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Abstract

The aims of the present study were to investigate the impact of rapamycin (RAPA) on the endometriosis (EMS) lesions in severe combined immunodeficiency (SCID) mice, and to examine the possible mechanism involved in a novel therapy in EMS. Following the successful establishment of an EMS-SCID mouse model, the mice were randomly assigned into the RAPA, control and saline treatment groups. Subsequent to treatment for 2 weeks, the serum hypoxia-inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF) were detected using ELISA. The levels of HIF-1α and VEGF, as well as the size of EMS lesions, were compared among the three groups. In addition, the HIF-1α, VEGF and CD34 protein expression levels, and the microvessel density (MVD) of the lesions were determined by immunohistochemical analysis. Compared with the control and saline groups, the volume of EMS lesions in the RAPA-treated SCID mice was significantly reduced. Furthermore, the serum level and protein expression of VEGF, and the MVD in the lesions of the RAPA-treated group were significantly reduced when compared with the other two groups. These parameters were comparable in the control and saline groups. In conclusion, RAPA may inhibit the growth of endometriotic lesions, most possibly through the inhibition of the expression of VEGF in lesions, thereby inhibiting angiogenesis.

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endometriosis

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