A NOVEL ANGIOGENESIS INHIBITOR BEVACIZUMAB
INDUCES APOPTOSIS IN THE RAT ENDOMETRIOSIS MODEL
Soysal D1,*, Kızıldağ S2,*, Saatlı B1, Posacı C1, Soysal S3, Koyuncuoğlu M4, Doğan ÖE1
*Corresponding Author: Sefa Kızıldağ, Ph.D., Dokuz Eylül University, Faculty of Medicine, 35340 İnciralti,
İzmir, Turkey. Tel.: +90-2324124613. Fax: +90-2322590541. E-mail:sefa.kizildag@deu.edu.tr
page: 73
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Abstract
Our aim was to investigate the effects of antivascular
endothelial growth factor (anti-VEGF) antibody
Bevacizumab on endometrial explants and
on apoptotic gene expression levels in the rat endometriosis
model. Endometriotic implants were
surgically formed, and rats treated with (i) 1 mg/kg
single subcutaneous injection of depot leuprolide
acetate; (ii) 2.5 mg/kg of single intaperitoneal injection
of bevacizumab; (iii) intraperitoneal injection of
saline. Histopathologic scores and adhesion scores of
endometriotic foci and levels of Bcl-2-associated X
protein (Bax), Cytochrome c (Cyt-c), B-cell lymphoma/
leukemia 2 (Bcl-2) and B-cell lymphoma-extra
large (Bcl-xl) mRNA gene expressions of endometriotic
foci. Bevacizumab treatment decreased the
endometriotic explant size compared with control.
Bevacizumab-treated rats had lower total adhesion
scores when compared with the control group. Semiquantitative
evaluation of the persistence of endometrial
epithelial cells in the explants showed a lower
score in gonadotropin-releasing hormone (GnRH)
agonist-treated rats compared with control rats. In
Bevacizumab increased expression of Bax 3.1-fold,
Cyt-c 1.3-fold and decreased expression of Bcl-2
0.4-fold, Bcl-xl 0.8-fold compared with the control
group. The GnRH agonist increased expression of
Bax 3.0 fold, Cyt-c 1.3 fold and decreased expression
of Bcl-2 0.4-fold, Bcl-xl 0.8-fold, compared with the
control group. This study suggests that a novel angiogenesis
inhibitor, anti-VEGF antibody bevacizumab
is as effective as GnRH agonist in the regression of
the endometriotic lesions in rat endometriosis model.
One possible mechanism of this effect is the induction
of apoptosis.
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