To explore the effect of hyperoside on insulin resistance in polycystic ovary syndrome rats by regulating adenosine monophosphate activated protein kinase (AMPK)/glycogen synthase kinase 3β (GSK3β) signaling pathway.

Nine female SD rats were randomly selected from 45 as the normal (NC) group (equal amount of distilled water), while the rest were used to construct a polycystic ovary syndrome model and grouped into model group (equal amount of distilled water), experimental-L group (0.7 mg·kg^-1·d^-1 hyperoside), experimental-H group (1.5 mg·kg^-1·d^-1 hyperoside), and inhibitor group (1.5 mg·kg^-1·d^-1 hyperoside and 0.2 mg·kg^-1·d^-1 Compound C), with nine rats in each group. The blood glucose meter was used to measure fasting blood glucose (FBG) in rats. Enzyme linked immunosorbent assay (ELISA) method was used to measure fasting insulin (FINS), testosterone (T), luteinizing hormone (LH), follicle stimulating hormone (FSH), estradiol (E2), triglycerides (TG), cholesterol (CHO), low-density lipoprotein (LDL), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α), and the homeostatic model assessment of insulin resistance (HOMA-IR) was calculated. Hematoxylin-eosin (HE) staining was used to detect pathological changes in ovarian tissue. Western blot was used to measure AMPK/GSK3β signaling pathway proteins in ovarian tissue.

The serum FBG levels in NC group, model group, experimental-L group, experimental-H group and inhibitor group were (5.54±0.69), (7.32±0.91), (6.65±0.82), (5.97±0.72) and (6.98±0.85) mmol·L^-1, respectively; the serum FINS levels were (9.58±1.39), (15.87±1.96), (13.65±1.62), (11.42±1.57) and (15.04±1.85) mU·L^-1, respectively; HOMA-IR indexes were 2.36±0.43, 5.16±0.71, 4.03±0.47, 3.03±0.52 and 4.67±0.68, respectively; the serum TG levels were (0.68±0.09), (1.58±0.18), (1.27±0.17), (0.98±0.13) and (1.46±0.18) mmol·L^-1, respectively; the serum CHO levels were (0.76±0.09), (1.52±0.18), (1.24±0.16), (1.01±0.14) and (1.41±0.17) mmol·L^-1, respectively; serum LDL levels were (1.62±0.23), (3.59±0.46), (3.06±0.42), (2.54±0.31) and (3.38±0.44) mmol·L^-1, respectively; serum LH levels were (4.21±0.57), (9.48±1.39), (7.86±0.96), (6.25±0.74) and (8.87±1.18) ng·mL^-1, respectively; serum FSH levels were (19.38±2.52), (8.27±1.05), (11.36±1.42), (14.65±1.76) and (9.57±1.48) ng·mL^-1, respectively; the serum T levels were (6.82±0.95), (13.86±1.62), (11.39±1.48), (8.98±1.14) and (12.64±1.53) ng·mL^-1, respectively; serum E2 levels were (1.02±0.14), (0.48±0.07), (0.72±0.09), (0.95±0.13) and (0.61±0.08) ng·mL^-1, respectively; the serum IL-6 levels were (53.46±7.69), (123.58±18.32), (98.39±13.58), (74.58±9.37) and (114.27±14.72) pg·mg^-1, respectively; serum TNF-α levels were (43.74±6.82), (82.19±10.46), (66.39±8.27), (51.72±7.24) and (73.54±1.02) pg·mg^-1, respectively; the relative protein expression levels of p-AMPK/AMPK in ovarian tissues were 0.79±0.11, 0.27±0.04, 0.49±0.07, 0.71±0.09 and 0.38±0.06, respectively; the relative protein expression levels of p-GSK3β/GSK3β were 0.19±0.04, 0.68±0.09, 0.47±0.07, 0.28±0.04 and 0.59±0.08, respectively. Among the above indexes, there were all statistically significant differences between NC group and modell group, model group and experimental-L group, experimental-L group and experimental-H group, experimental-H group and inhibitor group (all P<0.05).

Hyperoside improves insulin resistance in polycystic ovary syndrome rats by regulating AMPK/GSK3β signaling pathway.