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    Histopathological investigation of the effects of trastuzumab on the uterus in a rat model with endometriosis
    (2025) Kırıcı, Pınar; Annaç, Ebru; Deniz, Ömür Gülsüm; Kaplan, Selçuk
    It was aimed to investigate histopathological effects of trastuzumab on the uterus in a rat model with experimentally induced endometriotic tissue in the present study. In this study, 28 female Wistar albino rats (10-12 weeks old, 250-280 g) were divided into 4 groups (n =7). After a 7-day acclimation period, rats in the estrous phase were selected. The control group received no endometriosis induction; fat tissue was attached to the peritoneum and the abdomen was sutured. The endometriosis group underwent surgical induction of endometriosis using an auto-transplantation method, where uterine horn fragments were sutured to the peritoneum and mesentery. After a 4-week recovery period, the lesion size was measured, but no treatment was given. The endometriosis+Trastuzumab group received the same induction procedure as the endometriosis group, followed by intraperitoneal administration of trastuzumab (5 mg/kg) for 4 weeks. The trastuzumab group had no endometriosis induction but received the same trastuzumab dosage and schedule. Every animal tissue sample was obtained, and histopathological analysis was performed. In histopathological analysis, there was a significant difference between the Endometriosis group which had the most severe pathological changes compared to the control group (p<0.01). As well as; Endometriosis+Trastuzumab groups showed significant improvement in terms of epithelial integrity (p<0.05), Mast cell infiltration (p<0.01), glandular degeneration (p<0.05), and fibrosis (p<0.05), compared with the endometriosis group. In addition, no statistically significant difference was detected in the control and trastuzumab groups (p>0.05). Trastuzumab treatment resulted in protective effects on endometriosis-affected uterine tissue. In this context, histopathological results suggested that trastuzumab may be beneficial in treating damage caused by experimentally induced endometriosis.
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    The Effects of Nateglinide and Octreotide on the Uterus in Rats with Experimentally Developed Polycystic Ovary Syndrome: A Histopathological Study
    (2026) Kırıcı, Pınar; Annaç, Ebru; Deniz, Ömür Gülsüm; Kaplan, Selçuk
    Objectives: It was aimed to investigate the histopathological effects of Nateglinide (NG) and Octreotide (OC) on uterine morphology in rats with experimentally induced polycystic ovary syndrome (PCOS). Methods: Forty-two female Sprague-Dawley rats (10-12 weeks old, 340-360 g) were divided into six groups (n=7 per group) as Control, PCOS, PCOS+NG, NG only, PCOS+OC, OC only. PCOS was induced via daily oral administration of Letrozole (1 mg/kg) for 21 days. Treatment groups received NG (oral, 30 days) or OC (intraperitoneal, 0.1 mg/kg/day for 30 days). After the experiment, the uterus tissues of all rats were dissected and subjected to histopathological examinations after histological procedures. Results: Histopathological analysis revealed significant uterine damage in the PCOS group compared to other groups (P<0.01). In contrast, the Control, NG-only, and OC-only groups showed normal uterine architecture with intact epithelium, organized glands, and normal stromal structure and there were no significant differences between related groups (P>0.05). Treatment with NG or OC in PCOS rats led to improved epithelial and glandular morphology and reduced Mast cell density, no evidence of edema, and inflammation was found in the connective tissue of these treated groups, suggesting partial improvement of PCOS-induced uterine pathology (P<0.01). Conclusions: NG and OC treatments ameliorated PCOS-induced uterine histopathological changes, suggesting their potential to improve endometrial morphology. These findings may have implications for therapeutic strategies aimed at enhancing endometrial receptivity and highlighting the importance of addressing endometrial health in therapeutic strategies beyond ovarian treatment in PCOS patients.