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Updated: Apr 12, 2026
Mouse Model of Surgically-induced Endometriosis by Auto-transplantation of Uterine Tissue
Published on: January 6, 2012
Vascular endothelial growth factor receptor-2 inhibitor cediranib causes regression of endometriotic lesions in a rat
Fang Liu1, Li Wang1, Xian-Xia Zhang1
1Obstetrics and Gynecology Hospital, Fudan University 419 Fang-Xie Road, Shanghai 200011, PR China ; Department of Obstetrics and Gynecology of Shanghai Medical School, Fudan University 138 Yi-Xueyuan Road, Shanghai 200032, PR China ; Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases 413 Zhao-Zhou Road, Shanghai 200011, PR China.
Abstract:
Vascular endothelial growth factor (VEGF) receptor-2 plays an essential role in angiogenesis, and it also expressed in the glandular epithelium and stromal cells of ectopic endometrium. Cediranib is a protein tyrosine kinase inhibitor that potently inhibits VEGF receptor-2, but there is no study about its effects on the endometriosis. We induced endometriosis on both sides of the abdominal wall in 20 female Sprague-Dawley rats and randomly divided them into 2 groups. They were administered: cediranib 4 mg/kg/day (group 1), equal saline (group 2) for 12 days. Then, the lesion volumes were calculated, and Masson trichrome was used to detect fibrosis. Angiogenesis was evaluated by CD-31 immunohistochemistry and serum VEGF levels. Proliferation was indicated by proliferating cell nuclear antigen immunohistochemistry. Apoptosis was measured by a TUNEL assay and cleaved caspase-3 immunohistochemistry. In the treatment group, the lesion volumes were smaller (P < 0.05), and the degree of fibrosis was greater. The microvessel density was lower (P < 0.05) than control, however, serum VEGF was up-regulated by a negative feedback mechanism (P < 0.01). In addition, proliferation was significantly suppressed (P < 0.01), and apoptosis in the lesions was more obvious in the treatment group. These data indicated that cediranib can inhibit development of endometriotic lesions in rats.
Insights
Cediranib, a vascular endothelial growth factor receptor-2 inhibitor, effectively reduced endometriotic lesion size and suppressed proliferation in a rat model. The drug increased fibrosis and apoptosis, indicating potential therapeutic benefits for endometriosis.
Area of Science:
- Reproductive biology
- Pharmacology
- Oncology
Background:
- Vascular endothelial growth factor (VEGF) receptor-2 is crucial for angiogenesis and expressed in ectopic endometrium.
- Cediranib inhibits VEGF receptor-2 but its effects on endometriosis are unstudied.
Purpose of the Study:
- To investigate the effects of cediranib on the development of endometriosis in a rat model.
- To evaluate cediranib's impact on angiogenesis, proliferation, apoptosis, and fibrosis in endometriotic lesions.
Main Methods:
- Endometriosis was induced in Sprague-Dawley rats, divided into cediranib and saline groups.
- Lesion volume, fibrosis (Masson trichrome), angiogenesis (CD-31), proliferation (PCNA), and apoptosis (TUNEL, cleaved caspase-3) were assessed.
Main Results:
- Cediranib treatment significantly reduced endometriotic lesion volumes and microvessel density.
- Fibrosis increased, proliferation was suppressed, and apoptosis was enhanced in the cediranib group.
- Serum VEGF levels were upregulated via negative feedback.
Conclusions:
- Cediranib inhibits the development of endometriotic lesions in rats.
- Targeting VEGF receptor-2 with cediranib shows therapeutic potential for endometriosis.
