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Comparative Study
. 2010 Mar 1;93(4):1316-23.
doi: 10.1016/j.fertnstert.2008.10.056. Epub 2009 Jan 14.

Effect of pentoxifylline on vascular endothelial growth factor C and flk-1 expression on endometrial implants in the rat endometriosis model

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Free article
Comparative Study

Effect of pentoxifylline on vascular endothelial growth factor C and flk-1 expression on endometrial implants in the rat endometriosis model

Nikos F Vlahos et al. Fertil Steril. .
Free article

Abstract

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.

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