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 angiogenesis1,2. 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 steroidogenesis3,4,5.
Ziyodaxon Jaloliddinovna Ibragimova (Wed,) studied this question.