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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RESULTS
At the beginning of the medical treatment, the
mean surface areas of the endometriotic explants
were comparable in all three groups (GnRH agonist
group; 44.8 ± 39.2, bevacizumab group 2; 61.3 ±
41.1, control group; 48.4 ± 32.8, p = 0.412). After
treatment with saline solution there was no statically
significant change in mean explant size in the control
group (48.4 ± 32.8 mm2 vs. 45.9±33.7 mm2; p =
0.483). However, there was a statistically significant
decrease in the mean explant sizes 3 weeks after
treatment in both the GnRH agonist group (44.8 ±
39.2 mm2 vs. 16.3 ± 15.1 mm2; p = 0.008) and the
bevacizumab group (61.3 ± 41.1 mm2 vs. 22.1 ± 16.1
mm2; p = 0.005) (Figure 2). The decreases in the explant
sizes were 6.2, 61.9 and 58.8% for the control,
GnRH agonist and bevacizumab groups, respectively.
Bevacizumab treatment statistically significantly
decreased the endometriotic explant size (58.8%)
compared to the control group (6.2%) (p <0.001),
and this effect was comparable with the decrease in
GnRH agonist (61.9%) (p = 0.62).
Semiquantitative evaluation of the persistence of
endometrial epithelial cells in the explants showed a
significantly lower score in the GnRH agonist group
(0.56 ± 1.0) compared with the control group (1.78
± 1.0) (p = 0.009), but the bevacizumab-treated rats
(1.4 ± 1.4) had similar scores as the control group
(p = 0.445). There was no statistically significant difference
in semiquantitative evaluation between the
bevacizumab and GnRH agonist groups (p = 0.168).
The extent, severity and the total scores of the
adhesions were measured after the third laparotomy.
The severity, extent and total adhesion scores were
significantly reduced in the bevacizumab treated
group compared to the control group (p <0.05).
There were no statically significant difference between
GnRH agonist treated rats compared with the
control group and bevacizumab group (p >0.05) as
shown in Table 1.
In the PCR study of endometrial explants apoptotic
genes (Bax, Cyt-c) and anti-apoptotic genes
(Bcl-2, Bcl-xl) levels were evaluated (Table 2). In
endometrial explants bevacizumab statistically significantly
increased expression of the Bax gene 3.1-fold,
Cyt-c gene 1.3-fold and decreased expression of the
Bcl-2 gene 0.4-fold, Bcl-xl gene 0.8-fold compared with the control group (p <0.001). Similarly, GnRH
agonist statistically significantly increased expression
of the Bax gene 3.0-fold (p <0.001), Cyt-c gene 1.3-
fold (p <0.001) and decreased expression of the Bcl-2
gene 0.4-fold (p <0.001), Bcl-xl gene 0.8 fold (p =
0.002), compared with the control group. The level of
change in anti-apoptotic and apoptotic gene expressions
did not show statistically significant difference
between bevacizumab and GnRH agonist group in
endometrial explants (p >0.05). In the bevacizumab
and GnRH agonist groups, the ratios of Bcl-2:Bax
(0.13 and 0.14, respectively) and Bcl-2:Cyt-c (0.27
and 0.32, respectively) were decreased compared
with the control group (Table 3).
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