Related Experiment Video
Updated: Mar 18, 2026
Mouse Model of Surgically-induced Endometriosis by Auto-transplantation of Uterine Tissue
Published on: January 6, 2012
Effect of rapamycin on endometriosis in mice
X U Ren1, Yifeng Wang2, Gang Xu3
1Department of Obstetrics and Gynecology, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong 510282, P.R. China; Department of Obstetrics and Gynecology, Guangzhou Red Cross Hospital, Guangzhou, Guangdong 510120, P.R. China.
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.
Insights
Rapamycin (RAPA) significantly reduced endometriosis (EMS) lesion size in mice by inhibiting vascular endothelial growth factor (VEGF) and angiogenesis. This offers a potential novel therapy for EMS.
Area of Science:
- Reproductive Biology
- Immunology
- Pharmacology
Background:
- Endometriosis (EMS) is a debilitating gynecological condition.
- Current EMS treatments have limitations, necessitating novel therapeutic approaches.
- Understanding the molecular mechanisms driving EMS progression is crucial for developing effective therapies.
Purpose of the Study:
- To investigate the therapeutic effect of rapamycin (RAPA) on endometriosis lesions in a severe combined immunodeficiency (SCID) mouse model.
- To elucidate the underlying mechanism of RAPA's action in treating EMS, focusing on angiogenesis.
- To evaluate RAPA's impact on key angiogenic factors like vascular endothelial growth factor (VEGF) and hypoxia-inducible factor-1α (HIF-1α).
Main Methods:
- Establishment of an endometriosis-SCID mouse model.
- Random assignment of mice into rapamycin (RAPA), control, and saline treatment groups for 2 weeks.
- Quantification of serum HIF-1α and VEGF using ELISA.
- Immunohistochemical analysis of HIF-1α, VEGF, CD34 expression, and microvessel density (MVD) in lesions.
- Comparison of lesion volume and angiogenic markers among groups.
Main Results:
- Rapamycin treatment significantly reduced the volume of endometriosis lesions in SCID mice compared to control and saline groups.
- Serum VEGF levels and VEGF protein expression within lesions were significantly decreased in the RAPA group.
- Microvessel density (MVD) in the endometriotic lesions was significantly reduced following RAPA treatment.
- No significant differences were observed between the control and saline groups for any measured parameters.
Conclusions:
- Rapamycin (RAPA) demonstrates significant efficacy in inhibiting the growth of endometriosis (EMS) lesions.
- The primary mechanism of RAPA's action appears to be the inhibition of angiogenesis.
- RAPA achieves this by suppressing VEGF expression in endometriotic lesions, suggesting its potential as a novel therapeutic agent for EMS.
