Comparison of Surgically-Induced Endometriosis Models in Rats and the Role of VEGF: A Novel VEGF-Enhanced Rat Model of Endometriosis

In: Ahi Evran Medical Journal · 2026 · vol. 10(2) , pp. 212–222 · doi:10.46332/aemj.1798372 · W7204771960
article OA: diamond CC0
AI-generated summary by qwen3.7-flash, 2026-09-04

This study validates a VEGF-enhanced rat model of endometriosis that demonstrates superior angiogenesis and stromal development compared to standard surgical models, offering an efficient tool for investigating the disease's inflammatory and vascular characteristics.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

AI-generated deep summary by qwen3.7-flash, 2026-09-04 · read from full text

This study developed and validated a novel rat model of endometriosis by enhancing peritoneal endometrial tissue injection with vascular endothelial growth factor (VEGF). Forty female rats underwent oophorectomy and estrogen treatment, then were assigned to control or three surgical induction groups, including the VEGF-enhanced method. The results showed that the VEGF group exhibited extensive disease development with high stromal presence and angiogenesis, although it generated less estrogen receptor positivity than the Vernon-Wilson method. The authors conclude that this model is an efficient tool for studying endometriosis pathology despite the noted limitation in ER staining intensity. This paper is centrally about endometriosis — specifically the creation and validation of an animal model to study its pathological features.

Read from the paper's body, not the abstract. Not a substitute for reading the paper. No clinical advice. How this works

Abstract

Purpose: Endometriosis is an inflammatory disease characterized by the presence of endometrial tissue outside the uterine cavity. Animal models that reflect the characteristics of human disease have been critical for research in this field. We sought to develop and validate a novel rat model for endometriosis, incorporating vascular endothelial growth factor (VEGF) to enhance disease formation and explore disease-related characteristics.Materials and Methods: Forty adult female non-mated Wistar albino rats were divided into four groups: control, Vernon-Wilson method, peritoneal endometrial tissue injection, and peritoneal endometrial tissue injection with VEGF pre-treatment. All rats underwent oophorectomy to stabilize estrogen levels, followed by oral administration of 17β-estradiol for 21 days. Histopathological and immunohistochemical evaluations were performed to assessendometriosis severity, stromal development, CD10 positivity, estrogen receptor (ER) staining, VEGF staining, and inflammatory activity.Results: All three models generated significant differences compared to controls. The injection + VEGFgroup exhibited extensive endometriosis development, with higher epithelial density, stromal presence, andVEGF staining intensity compared to other groups, and similar overall endometriosis score to the Vernon-Wilson model. ER positivity was most pronounced in the Vernon-Wilson group, while stromal density and angiogenesis were higher in VEGF recipients.Conclusion: This study introduces a VEGF-enhanced rat model as an efficient and reproducible tool for studying endometriosis. This model emulates pathological features associated with endometriosis, including angiogenesis, immune response, and inflammation, but does not appear to generate ER positivity at the level of the Vernon-Wilson model. Despite this limitation, we believe this simple and efficient model can be crucial for researchers studying endometriosis.
Full text 4,157 characters · extracted from oa-doi-fallback · 6 sections · click to expand

Abstract

Purpose: Endometriosis is an inflammatory disease characterized by the presence of endometrial tissue outside the uterine cavity. Animal models that reflect the characteristics of human disease have been critical for research in this field. We sought to develop and validate a novel rat model for endometriosis, incorporating vascular endothelial growth factor (VEGF) to enhance disease formation and explore disease-related characteristics.

Materials and methods

Forty adult female non-mated Wistar albino rats were divided into four groups: control, Vernon-Wilson method, peritoneal endometrial tissue injection, and peritoneal endometrial tissue injection with VEGF pre-treatment. All rats underwent oophorectomy to stabilize estrogen levels, followed by oral administration of 17β-estradiol for 21 days. Histopathological and immunohistochemical evaluations were performed to assessendometriosis severity, stromal development, CD10 positivity, estrogen receptor (ER) staining, VEGF staining, and inflammatory activity.

Results

All three models generated significant differences compared to controls. The injection + VEGFgroup exhibited extensive endometriosis development, with higher epithelial density, stromal presence, andVEGF staining intensity compared to other groups, and similar overall endometriosis score to the Vernon-Wilson model. ER positivity was most pronounced in the Vernon-Wilson group, while stromal density and angiogenesis were higher in VEGF recipients.

Conclusion

This study introduces a VEGF-enhanced rat model as an efficient and reproducible tool for studying endometriosis. This model emulates pathological features associated with endometriosis, including angiogenesis, immune response, and inflammation, but does not appear to generate ER positivity at the level of the Vernon-Wilson model. Despite this limitation, we believe this simple and efficient model can be crucial for researchers studying endometriosis.

Keywords

Supporting Institution Project Number Ethical Statement

References

- Sanamiri K, Mahdian S, Moini A, Shahhoseini M. Non-hormonal therapy for endometriosis based on angiogenesis oxidative stress and inflammation. Int J Fertil Steril. 2024;18(4): 305–313. doi:10.22074/ijfs.2024.2012554.1547 - Maenhoudt N, De Moor A, Vankelecom H. Modeling endometrium biology and disease. J Pers Med. 2022;12(7):1048. doi:10.3390/jpm12071048 - Zheng P, Jia S, Guo D, et al. Central sensitization-related changes in brain function activity in a rat endometriosis-associated pain model. J Pain Res. 2020;13:95-107. doi:10.2147/JPR.S232313 - Grümmer R. Animal models in endometriosis research. Hum Reprod Update. 2006;12(5):641-649. doi:10.1093/humupd/dml026 - Tan Z, Hung SW, Zheng X, Wang CC, Chung JPW, Zhang T. What we have learned from animal models to understand the etiology and pathology of endometrioma-related infertility. Biomedicines. 2022;10(7):1483. doi:10.3390/biomedicines10071483 - Osteen KG, Yeaman GR, Bruner-Tran KL. Matrix metalloproteinases and endometriosis. Semin Reprod Med. 2003;21(2):155-164. doi:10.1055/s-2003-41322 - Ozer H, Boztosun A, Açmaz G, Atılgan R, Akkar OB, Kosar MI. The efficacy of Bevacizumab, Sorafenib, and Retinoic Acid on rat endometriosis model. Reprod Sci. 2013;20(1):26-32. doi:10.1177/1933719112452941 - McLaren J, Prentice A, Charnock-Jones DS, Smith SK. Vascular endothelial growth factor (VEGF) concentrations are elevated in peritoneal fluid of women with endometriosis. Hum Reprod. 1996;11(1):220-223. doi:10.1093/oxfordjournals.humrep.a019023 Details Primary Language English Subjects Clinical Sciences (Other) Journal Section Research Article Authors Selin Mutlu * 0000-0003-3200-5079 Türkiye Çağlar Yıldız 0000-0003-3150-3340 Türkiye Begüm Kurt This is me 0000-0002-7166-3130 Türkiye Neşe Yeldir 0000-0002-3812-6245 Türkiye Eren Cemal Mutlu 0000-0002-6072-8509 Türkiye Publication Date August 31, 2026 Submission Date October 6, 2025 Acceptance Date February 28, 2026 Published in Issue Year 2026 Volume: 10 Number: 2

Text is read by the "Ask this paper" AI Q&A widget below. Extraction quality varies by source — PMC NXML preserves structure cleanly, OA-HTML may include some navigation residue, and OA-PDF can have broken hyphenation. The publisher copy (via DOI) is the canonical version.

My notes (saved in your browser only)

Ask this paper AI returns verbatim quotes from the full text · source: oa-doi-fallback

Answers must be backed by verbatim quotes from this paper's full text. Hallucinated quotes are dropped automatically; if no verbatim passage answers the question, we say so. How this works

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (21)

Source provenance

openalex
last seen: 2026-09-10T06:07:16.079658+00:00
License: CC0 · commercial use OK