Treatment strategies with vitamin E and C in autologous intraperitoneal ovarian transplantation and its impact on ovarian surface epithelium and follicle reserve.

The objective of this study was to assess the impact of Vitamin E (Vit E) and Vitamin C (Vit C) on markers of the oxidant-antioxidant system, ovarian follicle reserves, and the surface epithelium in autologous intraperitoneal ovarian transplantation conducted in rats. The study aimed to investigate how these antioxidants influence various aspects related to transplantation outcomes, including oxidative stress markers, the preservation of follicle reserves, and the condition of the surface epithelium. A total of 20 adult female Wistar Albino rats were included in the study and randomly assigned to four different groups. Group 1, consisting of 5 rats, served as the control group and underwent a surgical procedure where their abdomens were opened and closed without any further intervention. Group 2, also consisting of 5 rats, underwent ovarian transplantation. In Group 3, comprising 5 rats, an intraperitoneal (IP) administration of 20 mg/kg body weight (b.w.) of Vitamin E (Vit E) was given 15 min prior to ovarian transplantation. Lastly, in Group 4, which included 5 rats, an IP administration of 50 mg/kg body weight (b.w.) of Vitamin C (Vit C) was given 15 min before ovarian transplantation. Vaginal cytology was performed in order to monitor the estrus phase in the rats. Biochemically, tissue and serum malondialdehyde (MDA) levels and erythrocyte superoxide dismutase (SOD) levels were measured. Histopathologically, the number of dysplastic changes in the ovarian surface epithelium and primordial, primary, secondary, Graaffian, and atretic follicles were examined. Dysplastic changes in the surface epithelium of Group 2 were found to be significantly higher than in Group 1 and 4 (p < 0.02). In Group 2, the ovarian follicle reserves (primordial, primary, secondary, and Graaffian follicles) were significantly lower than in other groups (p < 0.02). In addition, a significant decrease in SOD levels was found in Group 2 compared to other groups (p < 0.02). The study showed that Vit E and Vit C in autologous intraperitoneal ovarian transplantation preserved the ovarian follicle reserve. Vit C was found to be more effective than Vit E.

Propolis protects ovarian follicular reserve and maintains the ovary against polycystic ovary syndrome (PCOS) by attenuating degeneration of zona pellucida and fibrous tissue.

To examine the effects of 50 mg/kg and 150 mg/kg of propolis on ovarian folliculogenesis, p53 expression, and serum luteinising hormone (LH) and progesterone (P) levels in polycystic ovary syndrome (PCOS) modeled rats. Twenty-four Wistar female rats were divided into 4 experimental groups: Group 1 (G1, Control), Group 2 (G2, PCOS), Group 3 (G3, PCOS + 50 mg/kg propolis), and Group 4 (G4, PCOS + 150 mg/kg propolis). The PCOS model was induced via the administration of letrozole for 21 days. After 21 days, G3 and G4 received propolis (50 mg/kg or 150 mg/kg) by oral gavage for 10 days. Daily oestrous cycles were assessed to monitor PCOS formation. Histological examinations were carried out using haematoxylin and eosin (H&E) and Masson Trichrome (MT) staining. Ovarian follicles and corpus luteum (CL) structures were investigated. P and LH serum levels were determined by ELISA. A significant increase was observed in the number of cystic follicles in G2 compared to G1 (p < 0.001). Treatment with 50 mg/kg of propolis significantly ameliorated the elevated number of cystic and primary follicles seen in G2 (p < 0.001). Furthermore, G2 demonstrated a significant decrease in the number of CL structures (p < 0.05). Serum LH levels were significantly higher in G4 compared to both G1 and G2 (p < 0.01). No significant change was observed in circulating P levels. No p53 immunoreactivity was observed in any group. Low concentrations of propolis cannot completely improve the hormone profile and p53 expression associated with PCOS; however, these concentrations can control ovarian follicular cell architecture.