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Updated: Jun 26, 2026
Mouse Model of Surgically-induced Endometriosis by Auto-transplantation of Uterine Tissue
Published on: January 6, 2012
Effect of pentoxifylline on vascular endothelial growth factor C and flk-1 expression on endometrial implants in the
Nikos F Vlahos1, Odysseas Gregoriou, Aikaterini Deliveliotou
1Second Department of Obstetrics and Gynecology, University of Athens Medical School, Aretaieion Hospital, 76 Vas. Sofias Av., Athens 11521, Greece. nvlahos@jhmi.edu
Objective:
To investigate the effects of pentoxifylline, on vascular endothelial growth factor (VEGF)-C and flk-1 expression in the rat endometriosis model.
Design:
Prospective, randomized, placebo-controlled study.
Setting:
Academic institution.
Animal(S):
Twenty Wistar rats with surgically induced endometriosis.
Intervention(S):
Animals were evaluated after surgical induction of endometriosis and random allocation to a group that received pentoxifylline and a control group that received NaCl 0.9%, for 3 weeks. At the end of the treatment period the animals were killed and the implants evaluated macroscopically as well as by immunohistochemistry.
Main Outcome Measure(S):
Morphologic changes of the endometriotic implants; and evaluation of VEGF-C and flk-1 expression by a semiquantitative analysis (HSCORE) for the intensity of immunohistochemical reactivity.
Result(S):
A significant reduction was observed in the mean volume of the endometriotic implants per animal in the treatment group as compared with the control group. There was a significant reduction not only in the mean volume of implants per animal but also in the mean number of implants per animal after treatment. By immunohistochemical evaluation (HSCORE), there was a significant reduction in VEGF-C expression after treatment in all areas examined. A significant reduction of flk-1 expression was also noted in the glandular compartment after treatment but not in the epithelial surface or stroma.
Conclusion(S):
Pentoxifylline may cause suppression of endometriotic lesions by suppressing angiogenesis through VEGF-C and flk-1 expression.
