Steroid 5α-reductase 2 and StAR protein expression in ovaries of rats with polyendocrine metabolic ovarian syndrome.
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BACKGROUND: Polyendocrine metabolic ovarian syndrome (PMOS), formerly known as polycystic ovary syndrome, is characterised by hyperandrogenaemia, ovulatory dysfunction, and metabolic disturbances. Steroid 5α-reductase 2 (SRD5A2) converts testosterone to dihydrotestosterone (DHT), a potent androgen receptor agonist. However, the expression profile of SRD5A2 in the ovaries of women with PMOS and its potential contribution to hyperandrogenaemia remain unclear. The aim of this study was to investigate the expression of SRD5A2 and steroidogenic acute regulatory protein (StAR) in the ovaries of a rat PMOS model and to explore their associations with serum hormone levels. METHODS: Rats were randomly assigned to three groups: PMOS (n = 20), model control (dimethyl sulfoxide [DMSO]; n = 10), and blank control (BC; n = 10). The PMOS model was established via subcutaneous injection of dehydroepiandrosterone. Oestrous cycles were evaluated using vaginal cytology. Serum hormones were quantified using enzyme-linked immunosorbent assay. Protein and mRNA expression levels of SRD5A2 and StAR in ovarian tissues were evaluated using western blotting and reverse transcription polymerase chain reaction, respectively. RESULTS: Rats in the PMOS group exhibited significantly increased body weight (P < 0.05); disrupted oestrous cycles; and significantly elevated serum levels of anti-Müllerian hormone, testosterone, luteinising hormone (LH), and LH/follicle-stimulating hormone (FSH) ratio (P < 0.05). The protein and mRNA levels of SRD5A2 and StAR were significantly upregulated in the ovaries of the PMOS group compared with those of the BC and DMSO groups (P < 0.05). Ovarian volume and weight were similar among the groups, with no significant differences (P > 0.05). CONCLUSIONS: SRD5A2 and StAR are highly expressed in the ovaries of rats with PMOS and are associated with hyperandrogenaemia and elevated LH secretion. These findings indicate that SRD5A2 and StAR may contribute to PMOS pathogenesis, although further studies are required to establish causality.