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Aims: Estrogen (E2) deficiency has been related to uterine metabolic dysfunction, which could be accompanied by infertility in the reproductive ages. Despite having adverse effects, estrogen replacement therapy is considered the fundamental treatment strategy for this problem. The current study sought to determine the palliative effects of quercetin (Q) and vitamin E (Vit.E) on some of the uterine's metabolism-related factors in ovariectomized (OVX) rats and compare them with the effects of estrogen., Materials and Methods: Sixty-four rats were divided into eight groups. OVX animals were treated with Q (15 mg/kg/day), Vit.E (60 mg/kg/day), E2 (10 µg/kg/day), and Q (7.5 mg/kg/day) + Vit.E (30 mg/kg/day) for 10 weeks. Glucose and adiponectin were measured using glucose oxidase and ELISA, respectively. Furthermore, the present study investigated the alterations in the expression of AdipoR1, nesfatin1, and GluT4 genes., Results: Antioxidants suppress the weight gain of OVX animals. Also, Q, Vit.E, and E2 cause a significant decline in glucose and adiponectin levels ( p -value < .05). Finally, the expression of AdipoR1, nesfatin1, and GLUT4 genes was significantly increased in treated OVX rats' uterus., Conclusion: The present findings suggest that the administration of Q and Vit.E could demonstrate promising characteristics in a similar approach with estradiol and thus be considered as alternatives for estrogen replacement therapy.

The exact mechanisms of polycystic ovary syndrome (PCOS) are unknown and there is no effective cure for the disease. The aim of this study was to evaluate the alterations in serum oestradiol and adiponectin levels and in the expression of some important genes in the uterine and ovarian tissues of PCOS rats. The therapeutic effect of quercetin on PCOS was also assessed. Rats were divided into five groups: control, ethanol, quercetin (Q), PCOS and PCOS+Q. After 30 days of oral treatments, the rats' ovaries and uteri were removed and nesfatin-1, aromatase and adipoR1 expressions were quantified with real-time polymerase chain reaction. Serum adiponectin and oestradiol levels were evaluated using enzyme-linked immunosorbent assay technique. The results of this study showed that expression of nesfatin-1 and adipoR1 genes and adiponectin serum levels decreased in the PCOS rats, but aromatase expression and oestradiol level increased. Treatment with quercetin increased the adiponectin level and expression of adipoR1 and nesfatin-1 and decreased both the expression of aromatase and the oestradiol level. Quercetin improved PCOS by phytoestrogenic effects and mimicking oestrogen's function. Quercetin also affects important factors in both the uterus and ovary and could improve the obesity and the diabetic and infertility symptoms of PCOS.

Insulin resistance (IR) and infertility are two major complications of polycystic ovary syndrome (PCOS), which are the results of changes in certain parts of the reproductive and metabolic systems. We aimed to observe the effect of quercetin on dehydroepiandrosterone (DHEA)-induced PCOS and insulin resistance in rats. All animals were divided into five groups and DHEA was used to induce PCOS. Bodyweight and ovarian morphology of all groups were observed. Fasting blood glucose and insulin levels were analysed. The homeostasis model assessment of insulin resistance (HOMA-IR) method was used for IR level determination. The expression of oestrogen receptor α (ERα) and glucose transporter 4 (GLUT4) genes in the uterus was examined by real-time polymerase chain reaction. Liver hexokinase (HK) and glucokinase (GK) activity was determined using spectrophotometry. Quercetin significantly improved the IR state in PCOS rats. PCOS resulted in a decrease in liver GK and an increase in liver HK specific activity, whereas quercetin increased both liver HK and GK activity. Our data also showed a significant reduction in uterine ERα and GLUT4 expression in the PCOS group, which was increased by quercetin. A remarkable effect of quercetin was the intensive reduction of PCOS-IR and significant induction of uterine GLUT4 and ERα gene expression; it could thus be a possible effective treatment for PCOS and its complications, IR and infertility.

This study was designed to assess oxidative damage and cell apoptosis in the uterus of rats with streptozotocin (STZ)-induced diabetes. The role of vitamin E (VE) and/or folic acid (FA) in the protection from such damage was also evaluated. The treatments were performed for 4 weeks on six groups of rats: 1) normal control 2) diabetic control 3) diabetic rats receiving olive oil as a vehicle (without VE) 4) diabetic rats treated with VE (200 mg/kg) in olive oil 5) diabetic rats treated with FA (25 mg/kg) and 6) diabetic rats treated with VE+FA (200 and 25 mg/kg, respectively). We measured the malondialdehyde level (MDA), glutathione content (GSH) and the activity of GSH peroxidase (GPx), GSH reductase (GR) and catalase. Changes in caspase-3 activity were quantified in uterine tissue to assess the rate of apoptosis. In the rat uterine tissues, MDA content and caspase-3 activity were significantly elevated, while GPx, GR and CAT activities and the GSH level were significantly decreased in the diabetic control compared with those in normal rats (p<0.05). The combination of the vitamins (VE+FA) restored uterine GSH content and enzymatic activities of GPx, GR and CAT and reduced the MDA level (p<0.05). A prominent reduction in apoptosis of uterine cells was detected in diabetic rats treated with two vitamins (p<0.05). Overall, VE alone, not FA, produced results similar to those of the VE+FA combination. Thus, in the uterine tissue of diabetic rats, diabetes complications (that are caused by oxidative damage and apoptosis induction) can be prevented by the systemic administration of VE and FA.

The present study is the first attempt made to investigate the effects of diabetes on expression and promoter DNA methylation of TGF-β1, ESR-1, and CDH-1 genes and also the effects of folic acid (FA) and vitamin E (Vit E) supplementations on improving diabetes mellitus. STZ-induced diabetic rats were treated with Vit E (200 mg/kg/day) and FA (25 mg/kg/day) for 8 weeks and expression and DNA methylation of TGF-β1, ESR-1, and CDH-1 genes in uterus were analysed. Data indicated that diabetes increases the expression of TGFβ-1 and ESR-1 and decreases CDH-1 expression and TGFβ-1 promoter methylation in the uterus of rats. Vit E and FA improved the negative effects of diabetes by decreasing the expression of TGFβ-1 and ESR-1 and increasing that of CDH-1 in diabetic rats. In conclusion, these findings emphasise that Vit E and FA supplementations could improve negative effects caused by diabetes on uterus function and fertility in diabetic rats. [ABSTRACT FROM AUTHOR]

Background: Bioactivation of nitroglycerin (NTG) leads to the production of reactive oxygen species and reactive nitrogen species. The aim of this study was to investigate the effects of NTG treatment on the redox homeostasis in rat uterus around the time of implantation and the number of pups. Materials and Methods: The rats in long-term test groups were treated subcutaneously with NTG (15mg/kg BW) and normal saline (1ml/kg B) in control groups for 4 weeks. Afterwards, they were mated and divided into four groups. Two groups were treated until 5 days after mating. Thereafter, they were sacrificed and the activities of glutathione peroxidase (GPx), catalase (CAT), and glutathione reductase as well as the levels of reduced glutathione (GSH) and malondialdehyde (MDA) in the uterus homogenates were measured. In other two groups, treatments were continued until their pups were counted. In the short-term groups, treatments were started after mating, and all above parameters were measured as similar as long-term groups. Results: Long-term NTG treatment significantly increased MDA level and decreased the GPx activity and the pups number compared to the controls (p<0.05), whereas no marked alteration in the activities of GR and CAT and the levels GSH were observed. However, short-term NTG treated groups showed no significant changes in all the parameters mentioned above as compared with the controls. Conclusion: Long-term NTG treatment, unlike short-term treatment, may cause impaired implantation and infertility, but there is also room for further improvement. [ABSTRACT FROM AUTHOR]