Objective: Premature ovarian insufficiency (POI) is a heterogeneous condition described as the cessation of ovarian function in women below 40, often linked to oxidative stress. This study investigates the effect of caffeic acid (CA) on antioxidant capacity and histopathological changes in the ovaries of POI model mice.
Materials and methods: In this experimental study, 32 female mice were randomly divided into four groups (n=8): control, CA, POI, and POI+CA. POI was induced by daily injection of D-galactose (200 mg/kg) for six weeks. CA was administered intraperitoneally (IP) daily starting from the fifteenth day for four weeks (60 mg/kg). Finally, the mice were anesthetized, and their ovaries were collected after blood sampling. The levels of hormones (Follicle-Stimulating Hormone (FSH), Luteinizing Hormone (LH), and estradiol), oxidative stress markers (Total antioxidant capacity (TAC), Malondialdehyde (MDA), Glutathione peroxidase (GPx), and superoxide dismutase (SOD)), histopathological changes, and the expression of genes Nrf2, SOD1, and Gpx1 were evaluated.
Results: The results indicated that POI led to a significant increase in FSH, LH, and MDA levels (p<0.001) while decreasing SOD, GPx, and TAC levels compared to the control group (p<0.01). Additionally, the expression of Nrf2, SOD1, and Gpx1 genes was significantly lower in the POI group (p<0.01), and there was a notable reduction in the number of follicles compared to the control group (p<0.01). Caffeic acid treatment (POI+CA) significantly improved hormone levels, histopathological and oxidative stress factors, and related genes compared to the POI group (p<0.01).
Conclusion: The outcomes indicated that CA moderates the hostile effects of POI on the ovaries in mice by decreasing oxidative stress and increasing antioxidant defenses.