Platelet-rich plasma ameliorates cisplatin-induced premature ovarian insufficiency in rats by alleviating oxidative stress and granulosa cell apoptosis.

Premature ovarian insufficiency (POI) is a reproductive disorder characterized by impaired ovarian function. Cisplatin, a chemotherapeutic agent, is an important cause of acquired POI due to its ovarian toxicity, yet effective therapeutic interventions remain limited. Platelet-rich plasma (PRP) has gained increasing attention in regenerative medicine for its potential in tissue repair. This study investigated whether PRP could mitigate cisplatin-induced POI in rats and explored the underlying mechanisms. Female rats were randomly divided into control, cisplatin-induced POI, and CP+PRP groups. Ovarian function was assessed by serum hormone levels, estrous-stage patterns, ovarian morphology, ovarian index, and follicle counting. Oxidative stress levels and antioxidant capacity were assessed by measuring the levels of reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), and glutathione peroxidase (GSH-Px). Granulosa cell apoptosis was examined through immunohistochemistry for apoptosis-related proteins and TUNEL staining. PRP treatment partially improved ovarian function in cisplatin-induced POI rats, as evidenced by increased ovarian index, improved serum hormone profiles, more organized estrous-stage patterns, and preservation of follicular development. PRP also alleviated ovarian oxidative stress, as evidenced by reduced ROS and MDA levels and improved antioxidant capacity. Furthermore, PRP inhibited granulosa cell apoptosis, as demonstrated by decreased Bcl-2-associated X protein (Bax) expression, increased B-cell lymphoma 2 (Bcl-2) expression, and a reduced number of TUNEL-positive cells. These findings suggest that PRP may ameliorate cisplatin-induced POI in rats by alleviating oxidative stress and inhibiting apoptosis, providing experimental evidence for PRP as a potential therapeutic approach for chemotherapy-induced ovarian injury.