Preliminary Findings of Platelet-Rich Plasma-Induced Ameliorative Effect on Polycystic Ovarian Syndrome.
Cell J. 2019 Oct;21(3):243-252
Authors: Seyyed Anvari S, Dehgan GH, Razi M
Objective: Polycystic ovarian syndrome (PCOS) is characterized by hormonal imbalance, oxidative stress and chronic anovulation. The present study was designed to assess ameliorative effect of auto-locating platelet-rich plasma (PRP), as a novel method, for inhibiting PCOS-induced pathogenesis in experimentally-induced hyperandrogenic PCOS.
Materials and Methods: In this experimental study, 30 immature (21 days old) female rats were assigned into five groups, including control (sampled after 30 days with no treatment), 15 and 30 days PCOS-sole-induced as well as 15 and 30 days PRP auto-located PCOS-induced groups. Serum levels of estrogen, progesterone, androstenedione, testosterone, follicle stimulating hormone (FSH), luteinizing hormone (LH), ovarian total antioxidant capacity (TAC), malondialdehyde (MDA), glutathione peroxidase (GSH-px) and superoxide dismutase (SOD) were evaluated. Expression of estrogen receptor α (Erα), β (Erβ) and c-Myc were assessed. Finally, the numbers of intact follicles per ovary and mRNA damage ratio were analyzed.
Results: PRP groups significantly (P<0.05) decreased serum levels of FSH, LH, testosterone and androstenedione and remarkably (P<0.05) increased estrogen and progesterone syntheses versus PCOS-sole groups. The PRP auto-located animals exhibited increased TAC, GSH-px and SOD levels, while they showed diminished MDA content (P<0.05) versus PCOS-sole groups. The PRP auto-located groups exhibited an elevated expression of Erα and Erβ versus PCOS-sole groups. Moreover, PRP groups significantly (P<0.05) decreased c-Myc expression and mRNA damage compared to PCOS-sole groups, and remarkably improved follicular growth. Conclusion: PRP is able to regulate hormonal interaction, improve the ovarian antioxidant potential as well as folliculogenesis and its auto-location could be considered as a novel method to prevent/ameliorate PCOS-induced pathogenesis. PMID: 31210429 [PubMed]