Downregulation of miR-223 in a cyclophosphamide-induced mouse model of premature ovarian failure: histological and hormonal correlations

Premature ovarian failure (POF) is characterized by early ovarian dysfunction leading to infertility and hormonal imbalance. microrna-223 (MiR − 223) is a key microRNA that regulates multiple cellular processes, including inflammation, apoptosis, and follicular development. Emerging evidence suggests that dysregulation of mir-223 may play a role in ovarian pathology; however, its expression and function in chemotherapy-induced POF remain largely unexplored. This study aimed to investigate MiR − 223 expression in a cyclophosphamide-induced mouse model of POF and to explore its association with histological and hormonal alterations. Sixteen female mice were randomly assigned to control and POF groups. POF was induced via cyclophosphamide injection. Ovarian MiR − 223 expression was quantified by qRT-PCR, POF was confirmed by hematoxylin–eosin (H&E) histology, and serum FSH/LH levels were measured by ELISA. MiR-223 expression was significantly reduced in POF mice compared with the control group (0.068 ± 0.010 vs. 0.795 ± 0.041 relative fold expression units), corresponding to an approximately 11.7-fold decrease ( p < 0.001). The mean difference between groups was − 0.727 (95% CI: −0.759 to − 0.695), with a very large effect size (Cohen’s d = 24.36). Furthermore, serum FSH and LH levels were significantly elevated in the POF group compared with controls (both p < 0.001). Decreased MiR − 223 expression may contribute to ovarian dysfunction and could serve as a potential biomarker for further investigation in POF.