Exploration of the effects of hydrogen sulfide on steroidogenesis and histomorphology in the dehydroepiandrosterone-induced polycystic ovary syndrome rat model through histological and biochemical methods

Polycystic ovary syndrome is a disease that affects the reproductive, endocrine and metabolic systems. Hydrogen Sulfide is an endogenous gas that possesses intracellular signaling, angiogenesis, vasodilation, anti-inflammatory responses, antioxidant activities and anti-apoptotic processes. Our study is designed to investigate the effect of the H2S donor NaHS on anovulatory infertility, impaired follicular development and disrupted steroidogenesis mechanisms induced by DHEA. Thirty adult female rats were categorized into five groups: control, vehicle, PCOS, NaHS and PCOS+NaHS, respectively. The control group underwent no interventions. The vehicle group received a subcutaneous mixture of 0.01 ml 95% ethanol and 0.09 ml sesame oil. The PCOS model was created with subcutaneously administration of DHEA at a dose of 6 mg/100 g body weight. NaHS was administered intraperitoneally with a dose of 200 μg/kg/day. DHEA resulted in elevated serum E2 and serum progesterone levels, disturbance in the estrus cycle, a decrease in primordial, primary, Graafian follicle and corpus luteum numbers and an increase in secondary, cystic and atretic follicle numbers. It also increased apoptosis in follicles in parallel with the increase in atretic follicle numbers. DHEA has led to an increase in the protein and mRNA expressions of StAR, 3β-HSD and CYP19A1, while causing a decrease in the protein and mRNA expressions of CBS and CTH. The localization of CBS and CTH proteins in granulosa cells and oocytes has been identified. NaHS has reversed the disrupted estrus cycle, follicular damage and apoptosis induced by DHEA. It has reduced the increased expressions of StAR, 3β-HSD and CYP19A1 at both protein and mRNA levels and increased the decreased expressions of CBS and CTH at both protein and mRNA levels. In our study, we believe that NaHS reinstates the hormonal balance, prevents ovarian damage and corrects disorders in steroidogenesis.