Abstract

The objective of this study is to examine the impact of microRNA-320 on the phosphoinositide 3-kinase/protein kinase B signaling pathway in ovarian tissue and serum fasting serum insulin levels and homeostasis model assessment of insulin in rats with polycystic ovary syndrome. A total of forty-eight female Westar rats, characterized by their clean-grade health status, were allocated into three groups; Control, model, and microRNA-320 overexpression. Each group consisted of sixteen rats. In comparison to the control group, the model group exhibited elevated levels of fasting serum insulin levels, fasting blood glucose, homeostasis model assessment of insulin, testosterone, estradiol, and luteinizing hormone, while the level of follicle-stimulating hormone was reduced. Conversely, when compared to the model group, the microRNA-320 overexpression group demonstrated increased serum levels of testosterone, estradiol, and luteinizing hormone, accompanied by a decrease in follicle-stimulating hormone level. The microRNA-320 overexpression group exhibited a significantly greater quantity of small follicles and atresia follicles compared to the model group, while the presence of granular cell layer and corpus luteum was not observed. In comparison to the control group, the expression levels of phosphoinositide 3-kinase, protein kinase B, glucose transporter 4, forkhead box O3, and p27 in the ovarian tissue of the model group exhibited a significant decrease. Furthermore, when compared to the model group, the expression levels of phosphoinositide 3-kinase, protein kinase B, glucose transporter 4, forkhead box O3, and p27 in the ovarian tissue of the microRNA-320 overexpression group also demonstrated a significant decrease. Overexpression of microRNA-320 can significantly inhibit the expression of phosphoinositide 3-kinase/protein kinase B signaling pathway protein in ovarian tissue of polycystic ovary syndrome rats, and up-regulate the serum levels of fasting serum insulin levels and homeostasis model assessment of insulin.