Effect of rapamycin on endometriosis in mice

Ren,Xu; Wang,Yifeng; Xu,Gang; Dai,Libing

doi:10.3892/etm.2016.3280

Effect of rapamycin on endometriosis in mice

Authors:
- Xu Ren
- Yifeng Wang
- Gang Xu
- Libing Dai
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Affiliations: Department of Obstetrics and Gynecology, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong 510282, P.R. China, Department of Endocrinology, Guangzhou Red Cross Hospital, Guangzhou, Guangdong 510120, P.R. China, Department of Obstetrics and Gynecology, Guangzhou Red Cross Hospital, Guangzhou, Guangdong 510120, P.R. China
Published online on: April 20, 2016 https://doi.org/10.3892/etm.2016.3280
Pages: 101-106
Copyright: © Ren et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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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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