Placental-derived mesenchymal stem cells restore ovarian function and metabolic profile in the rat model for polycystic ovarian syndrome

Abstract

Abstract Introduction Polycystic ovary syndrome (PCOS) is an endocrine and metabolic disturbance that affects many women worldwide and is characterized by chronic anovulation, hyperandrogenism, and ovarian dysfunction. Infertility, insulin resistance, dyslipidemia, and liver dysfunction are perturbations induced by PCOS. Mesenchymal stem cells (MSCs) have recently emerged as a potential therapy for metabolic disorders such as PCOS due to their anti-inflammatory, antiapoptotic, proangiogenic, and proliferative properties. Placenta-derived mesenchymal stem cells (PDMSCs) are derived from the placenta and have advantages over other sources of MSCs in terms of availability, safety, and immunomodulation. Materials and Methods In this experimental study, we assigned twenty female Wistar rats into four groups (n = 5): control, sham, PCOS, and PCOS-PDMSCs. We induced PCOS in the rats by administering letrozole for 21 days. PDMSCs (1 × 106 cells) were injected through the tail vein. Fourteen days after cell infusion, we evaluated the number of healthy follicles, corpus luteum, and cystic follicles, as well as the levels of testosterone, follicle-stimulating hormone (FSH), luteinizing hormone (LH), fasting blood glucose, fasting insulin, and insulin resistance. Moreover, we measured the serum levels of cholesterol, triglyceride (TG), high-density lipoprotein (HDL), and low-density lipoprotein (LDL). Liver function was determined by evaluating aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels. Results The number of corpora luteum, primordial, primary, secondary, and antral follicles significantly elevated in the PCOS-PDMSCs group versus the PCOS group. The number of cystic follicles significantly decreased in the PCOS-PDMSCs group. LH and testosterone levels decreased significantly, while FSH levels increased significantly in the PCOS-PDMSCs group. Fasting blood glucose levels, fasting insulin levels, and insulin resistance notably decreased in the PCOS-PDMSCs group. The lipid profile improved in the PCOS-PDMSCs group with significant cholesterol, LDL, and TG decreases and an increase in HDL. The PCOS-PDMSCs group exhibited marked decreases in the AST and ALT levels. Conclusion Our results suggest that PDMSCs are a potential treatment option for PCOS because they can effectively restore folliculogenesis, correct hormonal imbalances, modify metabolic/lipid profiles, and alleviate liver dysfunction in a rat model of PCOS. However, further research is needed to establish the safety and effectiveness of PDMSCs for treating PCOS.