Effect of pentoxifylline on vascular endothelial growth factor C and flk-1 expression on endometrial implants in the rat endometriosis model.
OBJECTIVE
To investigate the effects of pentoxifylline, on vascular endothelial growth factor (VEGF)-C and flk-1 expression in the rat endometriosis model.


METHODS
Prospective, randomized, placebo-controlled study.


METHODS
Academic institution.


METHODS
Twenty Wistar rats with surgically induced endometriosis.


METHODS
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.


METHODS
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.


RESULTS
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.


CONCLUSIONS
Pentoxifylline may cause suppression of endometriotic lesions by suppressing angiogenesis through VEGF-C and flk-1 expression.
Vlahos
Nikos F
NF
Second Department of Obstetrics and Gynecology, University of Athens Medical School, Aretaieion Hospital, 76 Vas. Sofias Av., Athens 11521, Greece. nvlahos@jhmi.edu
Gregoriou
Odysseas
O
Deliveliotou
Aikaterini
A
Perrea
Despoina
D
Vlachos
Athanasios
A
Zhao
Yulian
Y
Lai
Joseph
J
Creatsas
George
G
D020533:Angiogenesis Inhibitors / Q000494:pharmacology; D000818:Animals; D004195:Disease Models, Animal; D004715:Endometriosis / Q000188:drug therapy / Q000378:metabolism* / Q000601:surgery; D004717:Endometrium / Q000187:drug effects / Q000378:metabolism / Q000637:transplantation*; D005260:Female; D007247:Infertility, Female / Q000188:drug therapy / Q000378:metabolism / Q000601:surgery; D010431:Pentoxifylline / Q000494:pharmacology*; D011446:Prospective Studies; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D019737:Transplants; D042582:Vascular Endothelial Growth Factor C / Q000096:biosynthesis*; D040301:Vascular Endothelial Growth Factor Receptor-2 / Q000096:biosynthesis*
D020533:Angiogenesis Inhibitors; D042582:Vascular Endothelial Growth Factor C; D040301:Vascular Endothelial Growth Factor Receptor-2; D010431:Pentoxifylline