The involvement of endometrial IGF-1R/IGF-1/Bcl-2 pathways and the potential regulatory effects of exogenously administrated melatonin on this expression is investigated in the experimental PCOS model in the present study. Thirty-two 6-8 week old Sprague Dawley rats were divided into four groups: the Sham Control Group (1% CMC/day by oral gavage [o.g.]); the Melatonin Group (2 mg/kg/day melatonin by subcutaneous administration [s.c.]); the Experimental PCOS Group (1 mg/kg/day Letrozole by o.g.); and the Experimental PCOS + Melatonin Group (1 mg/kg/day Letrozole by o.g. and 2 mg/kg/day melatonin by s.c. administration). Vaginal smear samples were taken from the 14th day to the end of the experiment for colpocytological measurements. At the end of the 21 day experimental period, uterine tissues were taken; Hematoxylin-Eosin histochemical, IGF-1R/IGF-1/Bcl-2, PCNA immuno-histochemical stainings and western blot analyses were performed for related antibodies. All of the data was supported statistically. The epithelium of endometrium lost its single-layer structure in some parts, separation was observed between the epithelium and the basal membrane junction, intracellular edema was found in the uterine glands by the polycystic ovary-induction. Also this induction increased the expression of IGF-1R/IGF-1, Bcl-2, and PCNA proteins. Morphological degenerations returned to its normal appearance generally by the melatonin administrations and melatonin also regulated the increased expression of endometrial IGF-1R/IGF-1/Bcl-2 and PCNA pathways. It is concluded that additional studies are needed, using melatonin as a supporting agent may be appropriate in cases of PCOS.
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