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

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. 45.933.7 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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