HISTOMORPHOLOGICAL AND MOLECULAR CHANGES IN OVARIAN TISSUE IN AN EXPERIMENTAL MODEL OF POLYCYSTIC OVARY SYNDROME-LIKE DISORDERS.

Ibragimova Ziyodaxon Jaloliddinovna

Authors

Ibragimova Ziyodaxon Jaloliddinovna Fergana medical institute of public health

Keywords:

polycystic ovary syndrome, ovary, folliculogenesis, insulin resistance, oxidative stress, inflammation, PI3K/Akt, aromatase, AMH, apoptosis

Abstract

This study investigated histomorphological and molecular alterations in ovarian tissue using a letrozole-induced rat model of polycystic ovary syndrome (PCOS). Forty immature female Wistar rats were randomized into control (n=20) and PCOS (n=20) groups. The model was induced with oral letrozole (1 mg/kg) for 21 days and validated by estrous cycle disruption, hormonal changes, and ovarian morphology. Results showed disrupted folliculogenesis with reduced preantral/antral follicles and increased atresia, stromal hyperplasia, fibrosis, and disorganized angiogenesis[1,2]. Decreased Ki-67 and increased Caspase-3 indicated impaired proliferation with enhanced apoptosis. Elevated TNF-α and IL-6 reflected chronic inflammation. Molecularly, CYP17A1 was upregulated, CYP19A1 downregulated, AMH increased, and PI3K/Akt signaling was impaired; oxidative stress (ROS, MDA) was elevated with weakened antioxidant defense.

In conclusion, PCOS-like conditions produce integrated morphological, cellular, and molecular disturbances that arrest follicular development and sustain anovulation. These findings support multi-target therapeutic strategies addressing insulin signaling, inflammation, oxidative stress, and steroidogenesis[3,4,5].

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