Investigation pathway of Nrf2/Keap-1 and some regulatory factors of antioxidants in patients with polycystic ovarian syndrome

Polycystic ovary syndrome (PCOS) is an endocrine disorder that affects approximately 10% of women worldwide. Oxidative stress (OS), caused by reactive oxygen species (ROS) in granulosa cells, plays an important role in the pathogenesis of PCOS. In this study, we investigated the levels of biomarkers involved in the formation of oxidative stress and antioxidant defense mechanisms. In our study, blood samples were taken from 55 patients diagnosed with PCOS and 45 healthy volunteers matched for age. Serum levels of Nuclear factor erythroid 2-related factor 2 (Nrf2), Keap1, Glycogen synthase kinase 3 beta (GSK-3β), NAD(P)H quinone oxidoreductase (NQO1), Glutathione-S-Transferase (GSTPi), Glutathione peroxidase (GSH-Px), Glutathione (GSH) and Sestrin-2 (Sesn2) were measured by enzyme-linked immunosorbent assay (ELISA) method. When the demographic data of patients and healthy individuals were examined, there was no statistically significant difference in terms of age, height, weight, body mass index (BMI), and waist circumference (WC) (p>0.05). In the statistical analysis, when the levels of NQO1, GSTPi, GSH, and Sesn2 were compared between PCOS and control groups, there was no statistically significant difference (p>0.05). GSH-Px and Nrf-2 levels were found to be significantly higher in the PCOS group than in the control group. Keap1 and GSK-3β levels were found to be significantly lower in the PCOS group than in the control group (p<0.05). In our study, it was observed that the Nrf2/Keap1 signaling pathway was effective in PCOS patients and stimulated the antioxidant defense system. In addition, Sesn2 also contributes to the antioxidant mechanism by stimulating the Nrf2/Keap1 pathway. The pathogenesis of the disease will be better understood with further studies to measure the gene expressions of these signaling elements involved in the antioxidant defense system.