Reproductive Sciences最新文献

This study compared the efficacy and safety of glucogan-like peptide-1 receptor agonists (GLP1RAs) combined with metformin versus metformin alone in women with polycystic ovary syndrome (PCOS). A systematic search of "PubMed", "EMBASE", "Cochrane Library", and "Web of Science", "Google Scholar" was conducted up to September 2024. Studies were included if they were RCTs investigating the combination of GLP1RAs and metformin in women diagnosed with PCOS. Eligible studies compared this combination therapy to metformin alone. Primary outcomes included changes in body weight, BMI, waist circumference, fasting glucose, HOMA-IR, androgen levels, and sex hormone-binding globulin (SHBG). Meta-analysis was performed using RevMan 5.4 software. Eight RCTs with a total of 337 participants were included. The combination of GLP1RAs and metformin resulted in significant reductions in body weight (mean difference [MD]=-1.37 kg, 95% CI [-2.07, -0.67]; P = 0.0001), BMI (MD= -0.88 kg/m², 95% CI [-1.37, -0.39]; P = 0.0005), waist circumference (MD= -2.46 cm, 95% CI [-3.59,-1.33]; P < 0.0001), fasting glucose level (MD= -0.30, 95% CI [-0.42,-0.17]; P < 0.0001), and glucose level at 2 h after OGTT (MD= -1.58, 95% CI [-2.10,-1.06]; P < 0.0001) compared to metformin alone. Improvements in insulin sensitivity (HOMA-IR) in GLP1RA + Met group were also observed (MD=-1.58, 95% CI [-2.10, -1.06]; P < 0.0001) comparing to Met group. Hormonal outcomes demonstrated an increase in SHBG (MD = 10.04, 95% CI [7.06, 13.01]; P < 0.0001). Adverse events were not different between GLP1RA + Met and Met groups. Collectivley, combination of GLP1RAs and metformin provides superior benefits over metformin alone in reducing body weight, improving insulin sensitivity, and regulating hormonal imbalances in women with PCOS.

Polycystic ovary syndrome (PCOS) is a prevalent endocrine and metabolic disorder affecting women of reproductive age. Oxidative stress (OS) is suggested to play a significant role in the development of PCOS. Using antioxidants to reduce OS and maintain a healthy balance in the body could be a novel treatment approach for PCOS. This study analyzed transcriptome data from the Gene Expression Omnibus database, focusing on genes associated with OS. By implementing two machine learning algorithms, three OS-related biomarkers-HMOX1, MMP9, and KLF2-were successfully identified. To evaluate the diagnostic potential of these biomarkers, a Logistic regression model was employed. Additionally, granulosa cells were collected from healthy individuals and infertile women with PCOS, and the reliability of HMOX1, MMP9, and KLF2 was verified by quantitative real-time PCR experiments. Furthermore, small molecule drugs targeting proteins encoded by genes HMOX1 and MMP9 were predicted through the Drug Signature Database. Molecular docking of drugs to proteins identified two antioxidants, butein and demethoxycurcumin, as potential candidates for PCOS therapy.

Polycystic Ovary Syndrome (PCOS) is among the most prevalent endocrinological abnormalities of young females, posing a grave public health challenge to the society. The objective of the present literature review is to analyze the enormous amount of information available by way of numerous multi-omic studies, and to explore a meaningful relationship between various factors such as genetic, proteomic, environmental etc. to understand the multifactorial metabolic disorder in a proper manner. Detailed literature search was done in various science article repositories and biomedical databases such as PubMed, Google Scholar, BioMed Central, Embase etc. by using several keywords in whole gamut of combinations. PCOS is a heritable disease. It manifests as a result of a combination of several intricately inter-linked symptoms such as anovulation, obesity, type II diabetes, hyperandrogenism, polycystic ovaries etc., the last one being the main manifestation of the disease, thus leading to infertility among several other complications. Such a multifactorial metabolic disorder with extreme symptomatic heterogeneity cannot be fully explained solely based on symptoms or genetic variations; thus, giving some space of thought to other factors such as epigenetic, microbiomic factors etc. playing a role in the causation of the disease. The present scientific survey of literature extensively reviews various aspects of PCOS by critically looking into the vast multi-omic data, and concluded with suggesting treatment options as well as lifestyle changes required to deal with the psychological/ emotional impacts of the condition on affected women.

Inguinal endometriosis is a less common form of endometriosis. Therefore, there is no consensus regarding its pathogenesis or treatment. In this study, we retrospectively reviewed the pathogenesis and treatment of six cases of inguinal endometriosis in our facility between 2009 and 2019. The pathogenesis of inguinal endometriosis is believed to involve hematogenous and lymphogenous extensions, as well as direct infiltration from the canal of Nuck or inguinal hernia. However, in our cases, the endometriotic lesions might have spread intravascularly from the uterine cavity. The lesions in our all cases were found as nodular or pointed hyperintensities on T1-weighted magnetic resonance imaging. In addition, all the patients experienced swelling and pain in the inguinal region during menstruation. Complete resection is often performed; however, hormonal therapy is administered to patients who do not undergo surgery, or to avoid recurrence. In our cases, dienogest was effective in reducing inguinal endometriotic lesions, improving pain, and preventing recurrence.

Polycystic ovary syndrome (PCOS) is a common cause of infertility in women, characterized by metabolic and hormonal irregularities. We investigated the effects of placenta-derived mesenchymal stem cells (PDMSCs) and platelet-rich plasma (PRP), as well as their combination on follicular development, hormonal profile, inflammatory parameters, and insulin resistance in a model of PCOS. In this study, 25 female Wistar rats were randomly allocated into five groups: Sham (given a dose of 1 mL of a 0.5% carboxymethylcellulose (CMC) solution), PCOS (administered 1 mg/kg of letrozole (LTZ) dissolved in CMC for 21 days), PDMSC (treated with a single intraovarian dose of PDMSCs), PRP (treated with a single intraovarian dose of PRP), and a combined PDMSC and PRP-treated group. After two weeks, serum and ovarian samples were collected for biochemical and histological analyses. Our results demonstrated that the simultaneous administration of PDMSCs and PRP had a synergistic effect compared to monotherapy, leading to an increase in estradiol (E2) and follicle-stimulating hormone (FSH) serum levels, a decrease in luteinizing hormone (LH) and testosterone levels, as well as inflammatory factors. Moreover, the combined therapy was associated with significantly lower levels of the homeostatic model of insulin resistance (HOMA-IR), fasting insulin (FINS), and blood glucose (FBG) compared to monotherapy. The combined treatment also caused a significant reduction in cystic follicles and an elevated number of corpus luteum, primordial, primary, secondary, and antral follicles. In conclusion, the combination of PRP and PDMSCs may have an ameliorative effect on modifying metabolic abnormalities and accelerating ovarian regeneration in PCOS.

Recurrent pregnancy loss (RPL), defined as two or more consecutive miscarriages before 20 weeks of gestation, affects 1-2% of couples worldwide. Pro-inflammatory cytokines, such as TNF-α, IL-1β and IL-6 play critical roles in early pregnancy, while anti-inflammatory cytokines like TGF-β and IL-10 promote immune tolerance to prevent harmful inflammatory responses that play important role in placental and fetal development. This aim of the study is to analyse the levels of inflammatory cytokines in blood serum from RPL patients and healthy women (control). The measured cytokines included TNF-α, IL-6, IL-10, TGF-β, CRP, ferritin, IL-1β and IL-4, IFN-γ and IL-17. Using an unpaired t-test and Pearson correlation, significant difference observed between the groups. The results had significantly elevated CRP levels with decreased levels of TGF-β and ferritin (p < 0.05), whereas, IL-1β and IL-4 also found raised indicating a link between systemic inflammation and recurrent miscarriages. IL-4 and CRP increase further suggest potential oxidative stress role in RPL cases. However, no significant differences observed in IL-10, IL-6, or TNF-α level between the groups. This study highlights immune dysregulation as possible contributors to early pregnancy loss, with significant increases in CRP, IL-1β, and IL-4 levels indicating an imbalanced immune response at the maternal-fetal interface. These cytokine elevations may disrupt immune tolerance, suggesting the need for further exploration into cytokine interactions in pregnancy and their potential as an investigatory biomarker and therapeutic target in RPL.

High-fructose and high-fat diet (HFHFD) has been associated with impaired spermatogenesis, leading to decreased sperm quality and increased male infertility, with similar effects observed in offspring. Cyanidin-3-O-glucoside (C3G), a recognized food antioxidant, has shown promise in protecting in male reproduction and modulating epigenetic modifications. However, its potential role in ameliorating intergenerational inheritance induced by HFHFD remains underexplored. In this study, we investigated the effects of paternal HFHFD on reproductive injury of offspring and the protective effect of C3G. Paternal mice were subjected to 12 weeks of HFHFD induction and C3G treatment was conducted for 8 weeks. Offspring obtained via in vitro fertilization were fed either a normal diet (ND) or high-fat diet (HFD). Our findings indicate that while the paternal HFHFD did not result in observable reproductive impairments in paternal mice, it did affect offspring testicular function through intergenerational inheritance, rendering them more susceptible to testicular damage and reduced sperm counts when exposed to an HFD. Notably, C3G intervention significantly mitigated these effects, suggesting its potential as a therapeutic compound for alleviating the impact of paternal intergenerational inheritance on male fertility resulting from HFHFD. These results underscore the importance of further exploring the mechanisms underlying intergenerational inheritance and the potential of interventions such as C3G in mitigating its effects, with implications for both basic research and clinical practice.

Melatonin is mainly synthesized and secreted by pineal gland, and plays multiple functions, including its regulating effects on reproductive processes. Sperm capacitation is necessary for fertilization, but the effect of melatonin on mouse sperm capacitation remains to be elucidated. We thus investigated the roles of melatonin on capacitation by culturing the sperms from mouse cauda epididymis in the medium with different doses of melatonin. The results showed that 10^-7 mol/L melatonin significantly enhanced the sperm capacitation by increasing the sperm tyrosine phosphorylation level, percentage of the capacitated sperms and intracellular calcium concentration. In addition, our in vitro and in vivo results showed that melatonin enhanced the fertilizing capacity by increasing the percentage of oocyte cleavage and the number of the fetuses from receptive females which were mated with melatonin-treated males. Mechanically, melatonin activated cyclic adenosine monophosphate (cAMP)/p-Protein kinase A (p-PKA) pathway. Furthermore, the melatonin-induced tyrosine phosphorylation of sperms was decreased by treatment of MT1 or PKA inhibitor. And the same result was found in the sperms cultured in non-capacitating medium (without bicarbonate and bovine serum albumin). Therefore, all those results indicate that MT1/cAMP/PKA pathway is one of key regulatory factors in melatonin-mediated sperm capacitation. The results here are crucial for understanding the molecular mechanisms by which melatonin regulates sperm capacitation, and providing theoretical support for controlling sperm capacitation during artificial insemination procedures.

Polycystic ovarian syndrome (PCOS) is a complex endocrine-metabolic disorder, and multiple factors contribute to its pathophysiology. The current study assessed a PCOS-like animal model induced by consuming a high-fat sugar (HFHS) diet and compared the treatment outcome of mitochondrial-targeted antioxidants versus heat therapy. Sixty rats were divided into the following study groups: three control groups (negative and positive for the treatments used), HFHS, hot tub therapy (HTT) treatment, and MitoQ10 treatment (500 µmol/L MitoQ10 in clean drinking water daily, from week fourteen till week twenty-two of the study). At week fourteen, PCOS was confirmed by vaginal smear examination; measurements of blood testosterone (T), anti-Mullerian hormone (AMH), follicle-stimulating hormone (FSH), luteinizing hormone (LH), glucose, and insulin; and determination of the homeostatic model assessment of IR (HOMA-IR). At week 22, blood samples were collected for measurement of the serum LH, FSH, AMH, T, insulin, glucose, lipid profile, kisspeptin, ADAM metallopeptidase with thrombospondin type 1 motif 19 (ADAMTS19), S100 calcium-binding protein B (S100B), fibulin 1 (FBLN1), immunoglobulin free light chains (FLCs), kappa and lambda. Ovaries were examined for morphological changes; for the levels of glutathione (GSH), catalase, SOD, malondialdehyde (MDA), and nitric oxide (NO); and the expression of FK506 binding protein 52 (FKBP52) and the androgen receptor (AR). The consumption of HFHS diet-induced PCOS-like features, which have been ameliorated by both HTT and mitoQ10 as potential therapies, with MitoQ10 showing a superior effect over HTT.