Table 1.
Characteristics of studies that reported the roles of quercetin in polycystic ovary syndrome
| Type of study | Authors/date | Source | Model | Results |
|---|---|---|---|---|
| Animal | Wang et al. 2017 [30] | China | 132 female Wistar rats (21 days old)/IR PCOS rat model/2 mL of quercetin solution (100 mg/kg)/ for 28 days | Quercetin treatment in the insulin-resistant PCOS rat model led to: |
| - 58.33% recovery rate of the estrous cycle, significant reduced the levels of blood insulin, interleukin 1β, IL-6, and tumor necrosis factor α. | ||||
| - Significant decreased the granulosa cell nuclear translocation of NF-κB | ||||
| - Inhibited the expression of inflammation-related genes, including the nicotinamide adenine dinucleotide phosphate oxidase subunit p22phox, oxidized low-density lipoprotein, and Toll-like receptor 4, in ovarian tissue. | ||||
| - IR improvement | ||||
| Jahan et al. 2018 [31] | Pakistan | Twenty-four adult female Sprague Dawley rats (60–70 days old and 180 ± 10 g body weight; randomly divided into four groups (n = 6–8))/quercetin (30 mg/kg) for 21 days. | By Quercetin administration: | |
| - No difference in mean body weight | ||||
| -Restoration of the estrous cycle | ||||
| -Significant decrease in ovarian diameter and in cystic follicle diameter | ||||
| -Number of ovarian follicles were declined as compared to untreated PCOS group | ||||
| -Counterbalanced the ROS levels and improved the antioxidant activities | ||||
| - Optimized the values of progesterone, estradiol, and testosterone levels when compared to control | ||||
| -Improvement of lipid profile (decreased cholesterol and triglyceride levels) and glucose levels. | ||||
| Neisy et al. 2018 [32] | Iran |
Thirty-five Sprague–Dawley female rats (DHEA-induced PCOS) randomly divided into five groups: (1) Control group, didn’t receive any treatment for 30 days; (2) quercetin (Q) group, treated with quercetin gavage (15 mg kg−1quercetin (3) ethanol vehicle group (ethanol gavage) for 30 days; (4) PCOS group (5) PCOSQ group (induced PCOS and then were treated with 15 mg kg− 1 quercetin for 30 days). 15 mg kg_1 quercetin for 30 days |
Quercetin significantly: | |
| -Improved folliculogenesis and luteinisation | ||||
| -Improved IR and decreased insulin levels | ||||
| -Increased activities of liver GK and HK | ||||
| ↑ Expression of uterine GLUT4 and ERa genes | ||||
| Shah et al. 2016 [33] | India | Forty-eight Sprague–Dawley female rats (3-week-old)/Quercetin (150 mg/kg, p.o.)/4 week. | Quercetin led to: | |
| - ↓ CYP17A1 gene expression | ||||
| - PI3 kinase inhibition | ||||
| -Decreased testosterone and LH levels | ||||
| -Significant improvement in insulin, testosterone, LH, and lipid profile (decreased HDL level was improved and significant reduction in serum cholesterol, triglyceride, LDL, and VLDL levels) | ||||
| -Significant improvement in the uterus histology | ||||
| -Improvement in cyst formation, folliculogenesis, and luteinisation | ||||
| - Did not modify body weight gain | ||||
| Hong et al. 2018 [34] | China | Sprague–Dawley female rats. (25 mg Quercetin /kg body weight for 4 week. | Quercetin led to: | |
| -Reversed the PCOS ovarian morphology. | ||||
| -↑ The levels and activities of antioxidant enzymes: CAT, SOD and GPX | ||||
| -Prevented weight gain | ||||
| -Caused significant decline in serum glucose | ||||
| -Normalized estradiol, testosterone levels, and steroidogenic enzyme activities in PCOS subjects | ||||
| -Blocked PCOS-related abnormalities and exerted protective effects on the ovary anatomy. | ||||
| Human | Rezvan et al. 2017 [35] | Iran |
84 women with PCOS (20–40 years old; and had the BMI of 25–40 kg/m2) randomly assigned to 2 groups. The treatment group received 1 g quercetin (two 500 mg capsules (Jarrow, USA) after each main meal (breakfast and lunch) for 12 weeks. The control group received placebo(2 capsules containing starch for 12 weeks) |
Quercetin led to: |
| -Increased the level of adiponectin by 5.56% and HMW adiponectin by 3.9% reduced the level of testosterone, LH, and HOMA-IR levels were also significantly reduced in quercetin group reduced of FBS, and insulin levels without changing BMI and WHR | ||||
| -Oral quercetin supplementation was effective in improving the adiponectin-mediated insulin resistance and hormonal profile of women with PCOS. | ||||
| Khorshidi et al. 2018 [36] | Iran |
78 overweight or obese women (25 ≤ BMI ≤ 40 kg/m2, 20–40 years) with PCOS 1000 mg/day quercetin or placebo for 12 weeks |
Quercetin led to: | |
| Decreased resistin plasma levels and gene expression, and testosterone and LH concentration | ||||
| No significant difference in SHBG levels | ||||
| FBG, fasting insulin, and insulin resistance were improved significantly in the quercetin group, but the changes were not statistically different compared with the placebo group | ||||
| Rezvan et al. 2018 [37] | Iran | 84 overweight or obese women with PCOS/1 g quercetin (two 500 mg capsules) daily for 12 weeks | Quercetin: | |
| Increased Adiponectin Receptors (ADIPOR1 and ADIPOR2) transcript expression by 1.32- and 1.46-fold respectively, | ||||
| Enhanced AMPK level by 12.3% |
Abbreviations: ADIPORs Adiponectin Receptors, AMPK AMP-activated protein kinase, BMI Body mass index, CYP17A1 Cytochrome P450 17A1, CAT Catalase, DHEA Dehydroepiandrosterone, Erα Oestrogen receptor α, FBG Fasting blood glucose, GK Glucokinase, GLUT4 Glucose transporter 4, GPX Glutathione peroxidase, HDL High-density lipoprotein, HK Hexokinase, HMW High molecular weight, HOMA-IR Homeostasis model of assessment-insulin resistance, IL-6 Interleukin 6, IR Insulin resistance, LDL Low-density lipoprotein, LH Luteinizing hormone, NF-κB Nuclear factor kappa-light-chain-enhancer of activated B cells, PCOS Polycystic ovary syndrome, PI3K Phosphatidyl inositol 3-kinase, ROS Reactive oxygen species, SHBG Sex hormone binding globulin, SOD Super oxide dismutase, TBARS Thiobarbituric acid reactive substances, VLDL Very low-density lipoprotein