International Journal of Reproductive BioMedicine
Volume:20 Issue: 10, Oct 2022

Psychological consequences of infertility could have a negative effect on marital and sexual satisfaction. Numerous medical associations have strongly recommended psychological interventions, including counseling, to help infertile couples. 

This study reviewed the effectiveness of counseling interventions on marital and sexual satisfaction in infertile couples.

This systematic review and meta-analysis was conducted according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses checklist, Databases including PubMed, Web of Science, Psych Info, Cochran Library, Scopus, and Embase were searched for relevant articles published up to March 2020. All randomized clinical trials assessing the impact of psychological interventions on marital and sexual satisfaction in infertile couples were included in the review. The outcome measures were marital and sexual satisfaction, and the pooled estimate of the effects was calculated using a random-effects model. The risk of bias was measured using the Cochrane risk of bias tool, and the summary measures were reported as 95% confidence interval and percentage of heterogeneity.

Out of the 309 studies found through the search, 13 randomized clinical trials including 230 infertile women and 512 infertile couples were systematically reviewed and included in the meta-analysis. It was found that counseling interventions improve marital and sexual satisfaction. 

As counseling and psychological interventions increase the marital and sexual satisfaction of infertile couples, those are highly recommended for the psychological management of infertile couples.

In vitro sperm preparation/incubation and cryopreservation are associated with oxidative stress as the main cause of sperm damage, and different strategies are used to improve sperm quality in in vitro conditions to treat male infertility. Growth factors (GFs) are biological molecules that play different roles in various cellular processes such as growth, proliferation, and differentiation. Many studies have shown that GFs and their receptors are expressed in the male reproductive system. In vitro supplementation of GFs to improve sperm parameters has yielded useful results. There are many studies on the effects of GFs on sperm quality improvement and subsequent assisted reproductive technology results. Hence, this study will review the in vitro results of various GFs including brain-derived neurotrophic factor, nerve growth factor, fibroblast growth factor, insulin-like growth factor I, and vascular endothelial growth factor to improve sperm quality.

Endometriosis is a multifaceted gynecological disorder defined as a benign estrogen-dependent chronic inflammatory process in which endometrial glands and stroma-like tissues are located outside the uterine cavity. It affects around 2-10% of all women during their reproductive years.  

This study aimed to evaluate the traffic of mesenchymal stem cells and inflammatory factors toward the lesions.

10 samples of normal endometrium and eutopic endometrium were studied as a control group and 10 ectopic samples were considered as a case group. Hematoxylin and eosin staining was used to evaluate stromal cells and inflammatory cells. Immunohistochemical staining was performed to show the presence of proliferating cell nuclear antigen in the lesions. The cells were digested and cultured in the laboratory to study cell proliferation. The number of cells and vessels were counted with Image J software, and data analysis was performed with Prism software.

Data analysis showed that the number of stromal cells and vessels in ectopic tissue were significantly higher than the control group (p < 0.001). Also, the number of inflammatory cells, including neutrophils, monocytes, lymphocytes, and macrophages, in the ectopic group was much higher than in the control group (p < 0.005).

By expanding the number of blood vessels, blood flow increases, and cell migration to tissues is facilitated. The accumulation of inflammatory cells, especially macrophages, stimulates the growth of stem cells and helps implant cells by creating an inflammatory process.

Although naproxen and diclofenac are the most commonly used nonsteroidal drugs, their toxicity affecting male reproductivity has not been sufficiently studied, particularly when used in pre-puberty.

This study aims to investigate the toxic effects of naproxen and diclofenac on sperm parameters and testes in pre-pubertal rats.

In this experimental study, 15 pre-pubertal male albino rats (aged 5 wk, weighted 70-80 gr) were used. The animals were divided in to 3 groups (n = 5/each) of control (0.1 ml dimethyl sulfoxide), naproxen (50 mg/kg), and diclofenac sodium (5 mg/kg), and were orally administered with these drugs every day for 3 wk. Epididymal spermatozoa were taken to assess sperm count, viability, and morphology. After preparing tissue sections, testicular histopathological and histomorphometric analyses were performed.

The body weights of rats in both naproxen and diclofenac groups significantly decreased (p < 0.001 and p = 0.03, respectively) in comparison to the control group. Remarkably, the testis weight and total sperm number significantly decreased (p = 0.002, and p = 0.004 respectively) in the naproxen-administered rats only. The sperm viability percentage decreased significantly in both diclofenac and naproxen-administered groups (p ≤ 0.001 and p = 0.03 respectively). Moreover, there was a significant increase (p < 0.001) in the percentage of sperm morphological anomalies in both drug-administered groups. Also, the histological and morphometric findings exhibited severe histopathological appearances in the testes and seminiferous tubules parameters in both drug-administered groups.

Naproxen and diclofenac administrations of rats before their puberty induce considerable harm to sperm parameters and testicular histology and morphometry. These severe toxic effects can lead to potential infertility.

Primary ovarian insufficiency (POI) is a rare disease clinically characterized by ovarian follicles depletion or dysfunction and menopause before the age of 40 yr as the cut-off age for POI. It is a complex disease, and its etiology involves several factors. However, genetic factors have a predominant role in the susceptibility to the disease.

This study aims to investigate the polymorphisms of rs243865 in the matrix metallopeptidase 2 (MMP2) gene and rs2234693 and rs9340799 in the estrogen receptor 1 (ESR1) gene with susceptibility to POI in Iranian women under 35 yr.

This case-control study was performed on 150 women with POI and 150 healthy women who were referred to Yazd Reproductive Sciences Institute, Yazd, Iran between May-October 2020. The genotyping of ESR1 rs9340799, rs2234693, and MMP2 rs243865 polymorphism was done using tetra-amplification refractory mutation system-polymerase chain reaction. In addition, haplotype analysis and linkage disequilibrium were investigated by SNPanalyzer software.

Our study revealed the frequency of rs243865 TT, CC genotypes in the MMP2 gene and rs2234693 CC, TT; and rs9340799 GG, AA in the ESR1 gene were more prevalent in the case group compared to the control group. In addition, ESR1 rs2234693 and rs9340799 genotypes showed significant association with the development of the disease in our population. Among 4 haplotypes for 2 polymorphisms in the ESR1 gene, rs2234693T/rs9340799A haplotype was associated with conferring risk to POI.

ESR1 rs2234693 and rs9340799 polymorphism were strongly associated with our population’s POI.

The relationship between the biochemical characteristics of follicular fluid (FF), oocyte quality and embryonic development has not yet been elucidated. We compared samples of FF with a normal metabolic profile against samples with metabolic abnormalities to identify potential predictive biomarkers of reproductive success.

To analyze peptide activity in the FF of women undergoing in vitro fertilization using 3 samples of FF per individual.

FF samples were obtained by ovum pick-up. Pathological samples were defined as samples of FF obtained from women with a gynecological condition or with infertility. A total of 30 women participated in this study. 3 samples of FF were obtained per individual (90 samples), but 8 samples were excluded because they were hemolyzed. The samples (n = 82 FF) included controls (n = 36, donors without fertility problems), women with endometriosis (n = 15), unexplained infertility (n = 19), and aged > 39 (n = 12). We assessed local encephalinergics: aminopeptidase-N (puromycin sensitive aminopeptidase and neutral endopeptidase; and components of the angiotensin system of the reproductive tract: prolyl-endopeptidase, APN, aspartate-aminopeptidase, and basic-aminopeptidase.

No differences were observed in peptide metabolism based on the presence or absence of oocytes in the FF. Women with endometriosis and aged > 39 yr showed alterations in puromycin sensitive aminopeptidase (p = 0.01), aminopeptidase-B (p = 0.01), aspartate-aminopeptidase (p < 0.001) and neutral endopeptidase (p < 0.001).

This study reveals alterations in the metabolism of enkephalin and angiotensin in pathological FF, which points to these components as potential diagnostic biomarkers.

According to stem cell theory, it seems that the proliferation/differentiation imbalance in endometrial mesenchymal stem cells (eMSCs) is the leading cause of endometriosis, so targeting them to modulate stemness-relevant factors seems to be a wise choice for endometriosis treatment.

We aimed to investigate the effects of metformin on stemness properties of eMSCs by evaluating the expression profile of stemness-related genes and microRNAs (miRNAs).

In this case-control study, MSCs were isolated from the eutopic endometrium of 3 endometriotic and 3 healthy women. After their characterization and culture, they were treated with 0.1, 1, and 10 mM metformin for 72 hr. Finally, the expression of octamer-binding transcription factor (OCT) 4A, OCT4B, OCT4B1, sex determining region Y-Box transcription factor 2, nanog homeobox, microRNA-200b, microRNA-145, and lethal-7b were analyzed by quantitative reverse transcription-polymerase chain reaction.

Metformin modulated the expression of stemness-related genes and miRNAs, OCT4A, OCT4B, OCT4B1, sex determining region Y-Box transcription factor 2, nanog homeobox, microRNA-200b, microRNA-145, and lethal-7b in eMSCs, especially at 1 and 10 mM concentration. Notably, metformin had a paradoxical effect on normal eMSCs.

We showed that metformin could modulate the expression of deregulated genes and miRNAs in faulty eMSCs, and restore their skewed self-renewal/differentiation balance, so it might be a promising drug for endometriosis treatment. The paradoxical effect of metformin on eMSCs and normal eMSCs might be because of their different metabolic patterns, so it requires further investigation to illustrate.

Endometriosis and infertility are caused by reactive oxygen species or free radicals, which promote endometrial cell growth and adhesion in the peritoneal cavity. Genistein has been proven to protect cells against reactive oxygen species by scavenging free radicals and decreasing the expression of genes-associated stress responses.

This study was conducted to determine whether genistein also acts as an antioxidant by elevating superoxide dismutase (SOD) and glutathione peroxidase (GPx) in the peritoneal fluid of the endometriosis mice model.

This experimental study involved 32 healthy female mice (Mus musculus), aged between 2-3 months and weighing 20-30 gr. They were divided into negative control group (healthy mice without genistein), endometriosis group (endometriosis mice without genistein), treatment group that was given different doses of genistein, that is, 0.13; 0.26; 0.52; 0.78; 1.04; and 1.3 mg/day (n = 4/each). SOD level in the peritoneal fluid was measured using the quantitative colorimetric determination method, and a colorimetric assay measured the GPx levels.

Results showed that the endometriosis model has lower SOD and GPx levels than the control group. The administration of genistein significantly normalized these changes. Genistein significantly increased SOD levels in the 0.13 mg and 0.26 mg treatment groups. Genistein also increased GPx levels significantly in all treatment groups.

Genistein increases SOD and GPx levels in the peritoneal fluid of an endometriosis mice model, and the change is dose-dependent.

The authors have been informed of an error that occurred on page 684 in which the number of participants should be replaced with 408 instead of 480. On behalf of the author, the publisher wishes to apologize for this error. The online version of article has been updated on 12 April 2021 and can be found at http://dx.doi.org/10.18502/ijrm.v17i12.5801