LAUSR

OBJECTIVE The aim of this study was to determine the impact of glycyrrhizin, an inhibitor of high mobility group box 1 (HMGB1), on glucose metabolic disorders and ovarian dysfunction in mice with polycystic ovary syndrome (PCOS). METHODS We generated a PCOS mouse model by using dehydroepiandrosterone (DHEA) plus high fat diet (HFD). 100 mg/kg glycyrrhizin was intraperitoneally injected into the PCOS mice and the effects on body weight, glucose tolerance, insulin sensitivity, estrous cycle, hormone profiles, ovarian pathology, glucolipid metabolism and some molecular mechanisms were investigated. RESULTS Increased number of cystic follicles, hormonal disorders, impaired glucose tolerance and decreased insulin sensitivity in the PCOS mice were reverted by glycyrrhizin. The increased HMGB1 levels in the serum and ovarian tissues of the PCOS mice were also reduced by glycyrrhizin. Furthermore, increased expressions of toll-like receptor (TLR) 9, myeloid differentiation factor 88 (MyD88) and nuclear factor-κB (NF-κB) as well as reduced expressions of insulin receptor (INSR), phosphorylated protein kinase B (p-AKT) and glucose transporter type 4 (GLUT4) were restored by glycyrrhizin in the PCOS mice. CONCLUSIONS Glycyrrhizin could suppress the PCOS-induced upregulation of HMGB1, several inflammatory marker genes and the TLR9/MyD88/NF-KB pathways, while inhibiting the INSR/p-AKT/GLUT4 pathways. Hence, glycyrrhizin is a promising therapeutic agent against PCOS.