ABSTRACT
Background: Paracrine disruption of growth factors in women with polycystic ovarian syndrome [PCOS] results in production of low quality oocyte, especially following ovulation induction. The aim of this study was to investigate the effects of metformin [MET], N-acetylcysteine [NAC] and their combination on the hormonal levels and expression profile of GDF-9, BMP-15 and c-kit, as hallmarks of oocyte quality, in PCOS patients
Materials and Methods: This prospective randomized, double-blind, placebo controlled trial aims to study the effects of MET, NAC and their combination [MET+NAC] on expression of GDF-9, BMP-15 and c-kit mRNA in oocytes [10 at the germinal vesicle [GV] stage, 10 at the MI stage, and 10 at the MII stage from per group] derived following ovulation induction in PCOS. Treatment was carried out for six weeks, starting on the third day of previous cycle until oocyte aspiration. The expression of GDF9, BMP15 and c-kit were determined by quantitative real time polymerase chain reaction [RT-qPCR] and western blot analysis. Data were analyzed with one-way ANOVA
Results: The follicular fluid [FF] level of c-kit protein significantly decreased in the NAC group compared to the other groups. Significant correlations were observed between the FF soluble c-kit protein with FF volume, and rostenedione and estradiol. The GDF-9 expression in unfertilized mature oocytes were significantly higher in the NAC group com- pared to the other groups [P<0.001]. Similar difference was not observed between the MET, NAC+MET and control groups. The c-kit expression in unfertilized mature oocytes were significantly lower in the NAC group compared to the other groups [P<0.001]. Similar difference was not observed between the MET, NAC+MET and control groups [Registration number: IRCT201204159476N1]
Conclusion: We concluded that NAC can improve the quality of oocytes in PCOS
ABSTRACT
Background: Reproductive toxicity is a major challenge associated with aluminum [Al] exposure. No studies have evaluated the possible effects of curcumin [CUR] on Al-in- duced reproductive dysfunction. Therefore, this study investigated the effects of CUR treatment on Al-induced reproductive damage
Materials and Methods: In this experimental study, 40 male Wistar rats were allocated to the five groups [n=8] based on the treatment they received: no treatment [control], solvent [dimethyl sulfoxide [DMSO] or distilled water], CUR 10 mg/kg body weight [BW], Al chloride 10 mg/kg BW, and CUR+A1 chloride [10 mg/kg BW/each alone]. Treatments were performed by intraperitoneal [IP] injections for 28 days. The left testis was assessed for histopathological analysis as well as the incidence of germ cell apoptosis. One-way analysis of variance [ANOVA] followed by the Tukey's test was used. PO.05 was considered significant
Results: Significant reductions in body and testis weight; plasma testosterone and luteiniz-ing hormone levels; sperm count, motility, morphology, and viability; germinal epithelium thickness; seminiferous tubules diameter; as well as, superoxide dismutase activity were observed in rats treated with Al. Moreover, Al exposure caused significant increments in the lumen diameter of tubules, terminal deoxynucleotidyl transferase dUTP nick end labeling [TUNEL]-positive cells and malondialdehyde [MDA] levels compared to the control group. However, in rats receiving CUR+A1, CUR significantly reversed the adverse effects of Al on testis and sperm quality. No significant differences in follicle-stimulating hormone ' - . [FSH] levels and nuclear diameter of spermatogonia were detected among all groups
Conclusion: It can be concluded that Al causes reproductive dysfunction by creating oxi-dative damage. CUR, on the other hand, reduces the toxic effects of Al and improves the antioxidant status and sperm quality in male rats
ABSTRACT
Leptin, a peptide hormone, is the product of [ob] Gene. Leptin regulate body weight and composition through reducing appetite and energy expenditure in rodents and humans. The aim of this study was to evaluate differences in expression of Leptin Gene in different tissues of streptozotocin induced diabetic rats. 40 Sprague Dawely rat were selected. Intra peritoneal injection was carried out in 20 rats and another 20 rats were used as control. After injection of 60mg/kg Streptozotocin, animals were transformed into diabetic. Glucose was measured by glucose oxidase method. Leptin and insulin were measure by commercially available immunoassay kits. After one week treatment, different tissues including adipose tissues, Spleen, epidydimis, and Liver of both control and experimental animals were dissected. For investigation of any changes of the Leptin gene expression in different tissues, RNA was extracted using Trizol method. By using RT-PCR technique, Leptin cDNA and beta-actin cDNA as internal control were constructed and PCR was carried out. The RT-PCR products were detected on 2% agarose gel using electrophoresis. Mean serum levels of Leptin was 5.23 +/- 0.45 ng/ml before injection of streptozotocin and markedly decreased in STZ induced diabetic rats to 0.79 +/- 0.25 ng/ml. This decrease was statistically significant [P<0.05]. There was a direct and significant correlation between leptin and insulin in streptozotocin-induced diabetic rats [r=0.37, P<0.05] while, this was reverse in control rats [r= -0.28, P<0.05]. Using RT-PCR method, Leptin gene expression in different tissues including fat epidydimis, liver, and spleen showed that the intensity of leptin band with 452 bp was decreased in diabetic rats in comparison to normal rats. Actin Gene expression was identified in PCR products having 403 bp and the intensity was constant in both groups. The reduction rates of [ob] mRNA in fat epidydimis tissue in STZ diabetic rats was remarkable in comparison to Spleen and Liver. It is speculated that Leptin gene could be under regulation of insulin dependent mechanism in diabetic rats and by modulating Leptin gene expression in diabetic patients, it may be useful in clinical practices