Mechanism of Platelet-Rich Plasma in Improving Cyclophosphamide-induced Premature Ovarian Failure in Rats

Background Premature ovarian failure (POF) is a clinical condition characterised by the cessation of ovarian function leading to infertility. Platelet-rich plasma (PRP) has attracted considerable attention in regenerative medicine. In this study, we aimed to evaluate the effectiveness of PRP in a rat model of POF induced by cyclophosphamide. Method Thirty 8–12-week-old female rats were divided into three groups: A, control group; B, model group (induced by cyclophosphamide); and E, intervention group (induced by cyclophosphamide + PRP). At the end of the experiment, body weight; ovarian parameters; and serum levels of the sex hormones, follicle-stimulating hormone (FSH), luteinising hormone (LH), oestradiol (E2), anti-Müllerian hormone (AMH), progesterone, and testosterone, were measured. Western blotting was used to detect the expression of related proteins, such as markers for germ cells, ovarian tissue angiogenesis, and granulosa cells, as well as cellular oxidative stress levels and DNA damage repair. Serum was used in proteomic and metabolomic analyses to cluster pathway networks of differentially expressed proteins and metabolites and conduct further correlation analyses. Result The levels of FSH, LH, E2, AMH, progesterone, and testosterone improved (p < 0.05) after POF rats received the PRP intervention. PRP also significantly increased the expression levels of the germ cell markers Ddx4, PCNA, and BMP4 in the ovarian tissues of POF rats, as well as the expression levels of the ovarian tissue generation and granulosa cell markers CD34, Bcl2, Caspase3, AMH, and FSHR (p < 0.05). PRP improved oxidative stress and mitochondrial and DNA damage in the granulosa cells of rats. Proteomic and metabolomics analyses revealed energy metabolism dysfunction in rats, and the inflammatory response was significantly alleviated after PRP intervention.