“…Several factors such as a gland/stroma ratio, the presence/absence of nuclear atypia, a high nuclear cytoplasmic ratio are examined in the evaluation/classification of the presence of endometrial hyperplasia in human-derived preparations [ 34 , 35 ]. However, our study was a rat study, and the histopathological evaluation of the preparations was performed by epithelial cell height and luminal epithelial cell height measurements based on the previous studies reported [ 15 , 36 , 37 , 38 , 39 , 40 ]. In our opinion, this evaluation gave us quantitative data creating the opportunity for statistical comparisons in the experimental models.…”
Section: Discussionmentioning
confidence: 99%
“…We calculated an average height by assessing the lowest and the highest regions. The measurements were taken under 40x magnification as previously described in the literature in micrometer units by a single-blinded pathologist (DK) ( Figure 3 ) [ 15 , 16 , 17 ]. Figure 2 Histopathologic evaluation of the uterine horns in terms of uterine hypertrophy/hyperplasia.…”
Endometrial hyperplasia is a process of endometrial proliferation that results in a thickening of the endometrial tissue. Melatonin might be able to change the pathophysiological process and prognosis into a positive way that might prevent and heal endometrial hyperplasia, which is the first stage of endometrial cancer.
For this perspective, we tried to investigate the effect of melatonin on uterine hypertrophy/hyperplasia in an experimental rat model. Forty Wistar-Albino rats were undergone bilateral oophorectomy and randomized into four groups. To create a model of uterine hypertrophy/hyperplasia in all groups, except the control group [C] (n = 10), 4 mg/kg/day estradiol hemihydrate were given for 14 days. The uterine hypertrophy/hyperplasia was evaluated histopathologically in the left uterine horns, then the groups were treated for 14 days as follows; melatonin (10 mg/kg/day/po) [M] (n = 10), melatonin + estradiol hemihydrate (10 mg/kg/day/po and 4 mg/kg/day/po) [M + E] (n = 10), and dark environment [D] (n = 10). Finally, the effects of the melatonin were examined histopathologically in the right uterine horns.
An uterine hypertrophy/hyperplasia model was established in all groups compared to the control group (p < 0.05). In the [M] and [M + E] groups, epithelial cell height and luminal epithelial cell height significantly decreased (41μm vs 12μm, p = 0.005; 14μm vs 10μm, p = 0.005, respectively for [M] group) and (32μm vs 14μm, p = 0.012; 17μm vs 10μm, p = 0.017, respectively for [M + E] group). The [D] group exhibited a significant decrease in epithelial cell height (33μm vs 20μm, p = 0.017).
With or without estrogen exposure, melatonin-treated and physiologically melatonin-released rats experienced a significant uterine hypertrophy/hyperplasia recovery. Melatonin may have protective effects on endometrial hyperplasia.
“…Several factors such as a gland/stroma ratio, the presence/absence of nuclear atypia, a high nuclear cytoplasmic ratio are examined in the evaluation/classification of the presence of endometrial hyperplasia in human-derived preparations [ 34 , 35 ]. However, our study was a rat study, and the histopathological evaluation of the preparations was performed by epithelial cell height and luminal epithelial cell height measurements based on the previous studies reported [ 15 , 36 , 37 , 38 , 39 , 40 ]. In our opinion, this evaluation gave us quantitative data creating the opportunity for statistical comparisons in the experimental models.…”
Section: Discussionmentioning
confidence: 99%
“…We calculated an average height by assessing the lowest and the highest regions. The measurements were taken under 40x magnification as previously described in the literature in micrometer units by a single-blinded pathologist (DK) ( Figure 3 ) [ 15 , 16 , 17 ]. Figure 2 Histopathologic evaluation of the uterine horns in terms of uterine hypertrophy/hyperplasia.…”
Endometrial hyperplasia is a process of endometrial proliferation that results in a thickening of the endometrial tissue. Melatonin might be able to change the pathophysiological process and prognosis into a positive way that might prevent and heal endometrial hyperplasia, which is the first stage of endometrial cancer.
For this perspective, we tried to investigate the effect of melatonin on uterine hypertrophy/hyperplasia in an experimental rat model. Forty Wistar-Albino rats were undergone bilateral oophorectomy and randomized into four groups. To create a model of uterine hypertrophy/hyperplasia in all groups, except the control group [C] (n = 10), 4 mg/kg/day estradiol hemihydrate were given for 14 days. The uterine hypertrophy/hyperplasia was evaluated histopathologically in the left uterine horns, then the groups were treated for 14 days as follows; melatonin (10 mg/kg/day/po) [M] (n = 10), melatonin + estradiol hemihydrate (10 mg/kg/day/po and 4 mg/kg/day/po) [M + E] (n = 10), and dark environment [D] (n = 10). Finally, the effects of the melatonin were examined histopathologically in the right uterine horns.
An uterine hypertrophy/hyperplasia model was established in all groups compared to the control group (p < 0.05). In the [M] and [M + E] groups, epithelial cell height and luminal epithelial cell height significantly decreased (41μm vs 12μm, p = 0.005; 14μm vs 10μm, p = 0.005, respectively for [M] group) and (32μm vs 14μm, p = 0.012; 17μm vs 10μm, p = 0.017, respectively for [M + E] group). The [D] group exhibited a significant decrease in epithelial cell height (33μm vs 20μm, p = 0.017).
With or without estrogen exposure, melatonin-treated and physiologically melatonin-released rats experienced a significant uterine hypertrophy/hyperplasia recovery. Melatonin may have protective effects on endometrial hyperplasia.
“…In terms of the use of less rats and ethical suitability, the A and B groups we used in our previous study were taken as control groups [5]. This study was also a pioneering study that showed the effect of nonionizing radiation on EH and we used exactly the same model in our study.…”
Section: Methodsmentioning
confidence: 99%
“…Group A ( n = 10): Not exposed to anything during the whole study period and used as the control group of the study model [5].…”
Section: Methodsmentioning
confidence: 99%
“…In experimental studies, it was pointed out that nonionizing radiation has genotoxic effects that may lead to carcinogenesis in many organ systems. In our previously conducted study, we have demonstrated the effect of nonionizing radiation in an experimental rat study and showed worsening of the disease in all investigated pathologic parameters, such as epithelial cell and luminal epithelial cell length and glandular density measurement [5]. In the EH treatment, progestin is the most commonly used drug [6].…”
<b><i>Objectives:</i></b> The aim of the study was to evaluate the negative effect of nonionizing radiation on the treatment of endometrial hyperplasia (EH) with oral progesterone. <b><i>Design:</i></b> Forty oophorectomized Wistar Albino female rats were included in this experimental rat study. <b><i>Materials and Methods:</i></b> The 4 groups were planned as follows: Group A; sham group; Group B; group receiving oral estradiol hemihydrate 4 mg/kg/day; Group C; 4 mg/kg/day oral estradiol hemihydrate followed with 1 mg/day medroxy progesterone acetate (MPA) and Group D; 4 mg/kg/day oral estradiol hemihydrate followed with 1 mg/day MPA with exposure to nonionizing radiation at 1800 mHz/3 h/day. After the experimental model, uterine horns were sampled and the preparations were evaluated for pathological parameters (glandular density, epithelial cell length, and luminal epithelial cell length) via light microscopy. Nonionizing radiation was created by a signal generator and a compatible mobile phone. <b><i>Results:</i></b> Estrogen was found to increase all parameters related to EH (<i>p</i> < 0.05). Progesterone treatment was found to decrease parameters related to EH (Group B vs. C; luminal epithelial cell length, glandular density, and epithelial length; 11.2 vs. 13.2 μm <i>p</i> = 0.007; 32.5 vs. 35.5, <i>p</i> = 0.068; and 219.9 μm vs. 285 µm, <i>p</i> < 0.001, respectively). Final analyses revealed reduced effectiveness of progesterone treatment in the rats exposed to nonionizing radiation (Group C vs. D); luminal epithelial cell length, glandular density, and epithelial length (11.2 μm vs. 13.5 μm, <i>p</i> = 0.179; 32.5 vs. 52, <i>p</i> < 0.001; and 219.9 μm vs. 374.1 μm, <i>p</i> = 0.001, respectively). <b><i>Limitations:</i></b> The limitations of our study are that the results of animal experiments may not be appropriate for direct adaptation to humans and the relatively low number of rats included in the study. <b><i>Conclusion:</i></b> Nonionizing radiation reduces the effect of progesterone in patients receiving treatment for EH.
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