This study aimed to assess the diagnostic and prognostic value of four biochemical markers-PAX9, HK10, TBX2, and CYFRA21-1-in ovarian carcinoma (OC).

Melatonin is multifaceted neurohormone secreted by pineal gland during darkness which is regulated by a small region present in hypothalamus i.e. Suprachiasmatic nucleus (SCN). Although melatonin primarily regulates the sleep and wake cycles, its effects are not limited to sleep. It also contributes to a number of physiological processes, including hormone regulation, metabolism, reproduction and body temperature regulation. Research has consistently highlighted the potential of melatonin to support reproductive health by enhancing testosterone synthesis, promoting gametogenesis, and improving both sperm quality and motility. Moreover, it has been found that melatonin improves fertilization rate and oocyte quality, making it a valuable adjunct in fertility treatments for both men and women. Beyond its role in reproductive function, melatonin also possesses potent anti-apoptotic, antioxidant, anti-inflammatory and properties. These effects help safeguard reproductive cells from the harmful impacts of oxidative stress and DNA damage, further underscoring melatonin's importance in maintaining optimal fertility and overall reproductive health. Despite its potential benefits, melatonin utility in reproductive health remains controversial due to inconclusive evidence, unclear mechanism and scattered information. Additionally, the supplementation of dosage and duration of melatonin in infertility and reproductive health needs exploration. In this review, we have tried to summarize the findings from various clinical and pre-clinical studies demonstrating the therapeutic potential of melatonin in male and female fertility and reproductive health. Aim of this review is to provide a deep knowledge on the current status of melatonin's potential therapeutic effects on reproductive health with emphasis on the molecular mechanism and future directions in melatonin's utility in reproductive health.

Varicocele, a condition of insufficient oxygen supply to testicular tissue leading to hypoxia, is a major factor contributing to male infertility. This study investigated the potential protective effects of N-acetylcysteine (NAC), a potent antioxidant, on sperm characteristics and hormonal receptor expression in a rat model of varicocele-induced testicular injury. Thirty-two adults male Wistar rats were randomly assigned to four groups: Sham, varicocele, varicocele with NAC treatment (varicocele + NAC), and NAC treatment only (NAC). Serum testosterone, LH, and FSH levels were measured, and sperm characteristics, testicular histology, and expression of some genes involved in sperm motility (Catsper-1 and Catsper-2), germ cell development (FSHR), and steroidogenesis (SF-1 and LHCGR) were evaluated in each group. Results revealed that varicocele significantly decreased serum testosterone levels, while simultaneously decreasing sperm quality, germ cell count, and expression of all the mentioned genes (P < 0.05). Also, the level of LH and FSH was significantly increased (P < 0.05). Notably, NAC treatment significantly improved sperm quality and protected testicular tissue against varicocele, suggesting its potential as a therapeutic agent for male infertility. This study demonstrates that NAC may offer a promising strategy for mitigating testicular damage induced by Varicocele.

Abnormal levels of Inhibin B (INH-B), a major regulator of ovarian activity, are closely linked to the development and prognosis of several ovarian disorders. Understanding the molecular mechanisms governing its regulation in granulosa cells is essential for both diagnosis and therapy. Our earlier work demonstrated the precise localization of lncPrep + 96 kb in granulosa cells and its central influence on the estrogen biosynthetic pathway. In this study, the impact of lncPrep + 96 kb on INH-B expression was investigated further. We created knockout mice lacking the long non-coding RNA lncPrep + 96 kb, which is specifically expressed in granulosa cells of the ovary. RNA sequencing revealed that the inhibin subunit βB (INHBB) was significantly elevated in knockout mice. ELISA was utilized to quantify INH-B levels in serum and granulosa cell supernatants, revealing a significant increase in knockout mice compared to wild-type controls. Overexpression of lncPrep + 96 kb fragments (2.2 kb and 2.8 kb) reduced INH-B expression. Endothelial differentiation-related factor 1 (EDF1), a key intracellular transcription factor, was found to be upregulated by lncPrep + 96 kb, resulting in decreased INH-B expression. In summary, lncPrep + 96 kb regulates INH-B secretion in granulosa cells by modulating of EDF1, providing new insights into the mechanism of INH-B expression and offering new research directions for diagnostic and therapeutic studies of abnormal ovarian functions.

Progesterone resistance is a key factor in the failure of conservative treatment in young endometrial cancer patients, and there is no effective method to predict and reverse progesterone resistance. CTMP is known to be involved in the development and progression of endometrial cancer, but the mechanism is unidentified. In this study, the immunohistochemical method was used to detect the expression of CTMP in the endometrium before and after progesterone treatment. In cell culture experiments, cell growth and proliferation were examined using CCK-8 and EDU incorporation assay. CTMP and PI3K/AKT pathway-related proteins expression were examined using Western blot. The results show that CTMP expression in the progesterone-resistant group of AEH was not significantly different from that in the progestin-sensitive group before treatment. There was no significant change in the expression of CTMP in the AEH progestin-resistant group, whereas there was a significant decrease in the expression of CTMP in the progesterone-sensitive group after treatment. CTMP knockdown enhances the sensitivity of endometrial cancer cells to medroxyprogesterone acetate (MPA) and may act by inhibiting the PI3K/AKT signaling pathway. This study confirms that CTMP may be associated with sensitivity to progestin therapy in endometrial atypical hyperplasia and endometrial cancer. CTMP may induce the development of progesterone resistance in endometrial cancer through activation of the PI3K/AKT signaling pathway.

Fetal hypoxia remains a major unresolved clinical challenge. Using artificial placenta (AP) technology, we established a standardized model of progressive hypoxia that induces brain injury in fetal sheep. To support the development of new antenatal monitoring strategies, we further profiled gestation-specific physiological, biochemical, protein, and cfRNA responses during progressive hypoxia. Seven fetuses at 123 days gestational age (dGA) and eight fetuses at 98 dGA (term = 150 dGA) were supported on the AP. Following a 12-h stabilization period, during which FiO₂ and gas flow to the AP oxygenator were adjusted to maintain fetal SO₂ at 65-75% and pCO₂ at 35-45 mmHg, both parameters were reduced by 5% every 30 min until termination criteria were met (arterial pH < 7.0 or base excess < -12). This protocol produced 240-300 min of progressive hypoxia. Physiological parameters, blood gases, biochemical markers, and cardiac and vascular ultrasound were assessed hourly. At the end of the experiment, brain histology and plasma cfRNA profiling were performed. Progressive hypoxia induced significant increases in pCO₂ and lactate and decreases in SO₂, CtO₂, pH, and BE in both groups (p < 0.05). Gestation-specific differences were observed in pO₂, glucose, and vital signs (heart rate, mean arterial pressure, and circuit flow). AST, ALT, and NSE rose significantly only at 123 dGA (p < 0.05), whereas S100B and NT-proBNP increased in both groups. Histology confirmed hypoxic brain injury at both gestational ages. In 123 dGA fetuses, iliac artery pulsatility index and heart rate predicted dysregulation of pH, BE, SO₂, and lactate (R = 0.538-0.745, p < 0.05). Plasma cfRNA analysis demonstrated distinct gestation-specific gene expression patterns consistent with hypoxia-induced injury. We developed a standardized, regulable model of fetal hypoxia and demonstrated brain injury accompanied by gestation-specific physiological, biochemical, and transcriptomic responses. Plasma cfRNA profiling highlighted its potential as an antenatal biomarker of hypoxic insult. This platform may facilitate the development of new diagnostic tools and guide evaluation of postnatal interventions.

Male infertility accounts for nearly half of all infertility cases globally, often resulting from oxidative stress and hormonal dysregulation. Conventional treatments offer limited efficacy, prompting interest in multi-target botanical therapies. This study evaluates a standardized polyherbal formulation (PHP), comprising Mucuna pruriens, Anacyclus pyrethrum, Asparagus racemosus, and Tribulus terrestris, for its protective effects against carbon tetrachloride (CCl)-induced reproductive toxicity. In vitro, assays confirmed the antioxidant capacity of PHP, with dose-dependent radical scavenging in DPPH and FRAP assays and inhibition of GC-1/GC-2 spermatogonia cell proliferation. In vivo, PHP administration (100, 300, 500 mg/kg) in carbon tetrachloride (CCl)-exposed rats significantly reduced oxidative stress, including a 52% reduction in thiobarbituric acid reactive substances (TBARS), 47% reduction in hydrogen perocide (HO), and normalization of enzymatic antioxidants glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), and peroxidase (POD); P < 0.01 vs. CCl. Hepatic injury biomarkedly improved, with alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), and total bilirubin levels reduced by 40-55% compared to CCl group (P < 0.01). PHP also restored reproductive hormones testosterone, luteinizing hormone (LH), follicle-stimulating hormone (FSH), and Prolactin levels elevated by 1.8 to 2.2-fold relative to intoxicated controls (p < 0.05). Gene expression analysis revealed significant recovery, with sex-hormone-binding globulin (SHBG), protein kinase B (AKT1), and androgen receptor (AR) transcripts upregulated 2.0-2.5-fold in PHP-treated animals (p < 0.05 vs. CCl), approaching control values. Histopathological analysis confirmed structural restoration of testicular architecture, with reduced seminiferous tubule degeneration and active spermatogenesis. In silico docking identified luteolin and acacetin as key phytochemicals. Luteolin exhibits strong binding to the androgen receptor (AR: -9.6 kcal/mol), AKT1 (-9.9 kcal/mol), and SHBG (-9.5 kcal/mol). It complied with Lipinski's rule of five and displayed favorable absorption, distribution, metabolism, excretion, and toxicity (ADMET) properties. Collectively, these findings suggest that PHP exerts multi-target protective effects against CCl-induced male infertility by mitigating oxidative stress, restoring hormonal balance, and modulating key reproductive signaling pathways. Further mechanistic and clinical investigations are warranted to validate its therapeutic potential.

This study aims to investigate the genetic associations of endometrial cancer (EC), ovarian cancer (OC), and cervical cancer (CC), identify potential key genes using multiple genomic analysis approaches, and analyze their roles in cancer development.

Uteroplacental insufficiency (UPI) disrupts fetal brain development and induces oxidative damage. This study evaluates the neuroprotective effects of ferulic acid (FA) on oxidative stress biomarkers, neuroinflammation, the Akt/GSK-3β signaling pathway, and neuronal density in the medial prefrontal cortex (mPFC) following UPI in rats. Twenty pregnant Wistar rats were randomly assigned to four groups: Control, Sham Surgery, UPI + Vehicle (UPI + normal saline), and UPI + FA (UPI + FA at 100 mg/kg). UPI was induced via permanent ligation of the uterine arteries on embryonic day (ED) 18. FA or normal saline was administered orally from ED14 to ED21. On ED21, fetal brain tissue was analyzed for oxidative stress biomarkers (8-hydroxy-2'-deoxyguanosine, protein carbonyl, 4-hydroxy-2-nonenal, and malondialdehyde), inflammatory cytokines (interleukin-6 [IL-6], IL-1β, tumor necrosis factor-alpha [TNF-α], and IL-10), Akt/GSK-3β gene expression, and neuronal density in the mPFC. FA treatment significantly reduced oxidative stress biomarkers and pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α) while decreasing GSK-3β expression and increasing Akt expression. Additionally, FA enhanced neuronal density in the mPFC and elevated IL-10 levels compared to the UPI + Vehicle group (p < 0.05). Pre-treatment with FA prior to UPI induction mitigated oxidative stress, modulated the Akt/GSK-3β signaling pathway, suppressed neuroinflammation, and preserved cortical integrity in the fetal brain.

Polycystic Ovary Syndrome (PCOS) is a complex endocrine and metabolic condition that affects around 8-13% of women worldwide. PCOS is defined by hyperandrogenism, insulin resistance, and many reproductive irregularities, providing significant challenges with diagnosis and treatment. Here thoroughly analyzes the many animal models used to conduct PCOS research, focusing on their mechanisms, benefits, and drawbacks. Multiple models, including those influenced by androgens (testosterone and DHEA), estrogen, aromatase inhibitors (such as letrozole), and progesterone receptor antagonists (like RU486), are examined for their capacity to recreate the clinical characteristics of PCOS. Although animal models are frequently employed for their cost-efficiency and simple handling, they provide difficulties in correctly replicating human physiology due to variations in reproductive biology. The research highlights the importance of advanced animal models that represent the complete range of PCOS symptoms seen in humans. Furthermore, it emphasizes the significance of these models in understanding the pathophysiology of PCOS and in developing beneficial therapeutic approaches. Future research must concentrate on improving current models and investigating novel approaches for a more accurate depiction of this complex disease to optimize translational results in clinical conditions.

To investigate the pathogenicity of splice-site variants in DNAH17, and analyze their impact on sperm morphology and motility, we employed whole-exome sequencing (WES) and Sanger sequencing to identify and validate candidate variants. Computational predictions of splicing defects were performed using varSEAK and MobiDetails. Functional validation was conducted using minigene splicing assays in HEK293T cells. Structural modeling of mutant proteins was performed with AlphaFold3 and visualized by PyMOL. Two novel splice-site variants (DNAH17: c.11677 + 5G > T/c.11677 + 5G > A) were identified in a proband with asthenozoospermia and multiple morphological abnormalities of the sperm flagella (MMAF). Bioinformatics tools predicted disruption of the canonical donor splice site (MaxEntScan score reduction: 54.2% for G > A, 39.5% for G > T; SpliceAI donor loss scores > 0.8). Minigene assays confirmed exon 72 skipping, leading to a frameshift mutation (p.Asn3844Lysfs*13) that truncates the AAA6 domain. This study expands the mutational spectrum of DNAH17-related male infertility by demonstrating that splice-site variants disrupting the AAA6 domain represent a novel pathogenic mechanism underlying asthenozoospermia and MMAF. These findings underscore the necessity of integrating splice-site analysis into genetic diagnostics for male infertility.

Ovarian tissue vitrification is a key strategy for fertility preservation, but remains hindered by oxidative damage and compromised tissue viability. This study evaluates the cytoprotective effects of glutathione (GSH) supplementation during the vitrification of mouse ovarian tissue, including autologous transplantation experiments. Mice ovaries were cryopreserved with 0, 2, 4, or 8 mM GSH, followed by comprehensive histological, biochemical, and molecular assessments, as well as autologous transplantation to assess functional recovery. GSH, particularly at 4 mM, significantly preserved follicular architecture, enhanced antioxidant enzyme activity, attenuated mitochondrial dysfunction, DNA damage, and apoptosis, and suppressed pro-inflammatory and fibrotic signaling pathways. GSH also restored angiogenic markers and improved endocrine function in ovarian grafts after autologous transplantation, as evidenced by ameliorative levels of estradiol, progesterone, anti-Müllerian hormone (AMH), luteinizing hormone (LH), and follicle-stimulating hormone (FSH). These findings support GSH as a potent adjuvant for improving ovarian tissue vitrification outcomes and warrant further translational evaluation in fertility preservation protocols.

Preeclampsia (PE) is a hypertensive disorder of severe pregnancy complication characterized by placental dysfunction and systemic inflammation. Resveratrol (RES), a natural polyphenol, has been shown to exert anti-inflammatory effects partly through the activation of SIRT1. NLRP3 inflammasome-mediated pyroptosis plays a crucial role in placental inflammation. This study aims to investigate the role of RES in regulating trophoblast pyroptosis through SIRT1 activation in PE. Placental tissues from PE patients and normal pregnancies were analyzed for SIRT1 and pyroptosis markers. A lipopolysaccharide (LPS)-induced PE mouse model and HTR-8/SVneo trophoblasts model were used to examine for pyroptosis following RES treatment. Placental tissues from PE patients exhibited significantly reduced SIRT1 expression and elevated pyroptosis markers (NLRP3, Caspase-1) compared to normal pregnancies. In a LPS-induced PE mouse model, RES treatment ameliorated pregnancy outcomes by reducing blood pressure, proteinuria, and improving renal morphology. RES also enhanced fetal and placental development, as evidenced by decreased embryo resorption rates, increased fetal weight, and improved spiral artery remodeling. Mechanistically, RES upregulated SIRT1 expression and suppressed pyroptosis-related proteins (NLRP3, Caspase-1, GSDMD, ASC) in placental tissues of PE mice. In vitro, RES attenuated LPS-induced trophoblast dysfunction by enhancing proliferation, migration, and invasion in HTR-8/SVneo cells. This was accompanied by SIRT1-mediated suppression of pyroptosis and reduced secretion of inflammatory cytokines (IL-18, IL-1β). These findings demonstrate that RES activates SIRT1 to inhibit trophoblast pyroptosis, thereby improving placental function and pregnancy outcomes in PE. This study highlights RES as a potential therapeutic agent for PE by modulating SIRT1-mediated pyroptosis pathways.

The "double-edged sword" effect of dexamethasone on fetal development has attracted significant attention. Currently, the "one-size-fits-all" prenatal corticosteroid regimen fails to confer uniform benefits to all pregnant women and fetuses. Simultaneously, there exist controversies regarding the wide time window for administration and the insufficient consideration of individual factors in dosage selection. Therefore, this study aimed to establish a precise prenatal dexamethasone exposure (PDE) mouse model that closely mimics clinical use, to evaluate its effects on placental morphology, development, differentiation, vascular formation, and nutrient transporter function. Dexamethasone was injected subcutaneously at diverse gestational stages, doses, and courses. The late-stage, high-dose, single-course PDE exhibited the most pronounced effects, including reduced placental weight, a decreased labyrinth-to-junctional zone (LZ/JZ) ratio, impaired trophoblast proliferation and differentiation, increased apoptosis, and decreased vascular endothelial growth factor (VEGF) expression. Amino acid and cholesterol transporter levels increased in both sexes, whereas glucose transporters showed sex-specific alterations-elevated in males but reduced in females. Further investigation revealed that PDE suppressed the "glucocorticoid (GC)-insulin-like growth factor 1 (IGF1) axis" programming, which was highly correlated with placental development and function indicators. In conclusion, PDE induced alterations in placental morphology, development, and nutrient transport function, which were influenced by stages, doses, courses, and sex differences. These changes may be associated with the "GC-IGF1 axis" programming. This study provides experimental and theoretical evidence to more precisely guide the clinical application of prenatal dexamethasone.

Endometriosis is a prevalent chronic inflammatory condition impacting 5-10% of reproductive-age women, commonly resulting in debilitating pelvic pain and infertility. Despite extensive research efforts, the precise underlying pathophysiology remains largely unclear. Emerging evidence increasingly suggests that cellular senescence, iron overload, and fibrosis collectively form a critical pathological axis that significantly contributes to the persistence and severity of the disease. However, the intricate mechanistic interplay between the immune system's failure to effectively clear senescent cells, the damaging effects of iron-induced oxidative stress, and the subsequent fibrotic remodelling is still poorly understood. This narrative review highlights the interconnected roles of impaired immune clearance of senescent cells, iron accumulation, and fibrosis development in driving endometriosis pathogenesis. The review aims to clarify how iron overload and cellular senescence contribute to the progression of endometriosis. It also evaluates novel therapeutic strategies that target iron dysregulation and senescence pathways. By exploring this detrimental triad, we seek to identify potential new avenues for transforming the management of endometriosis, offering hope for more effective treatments to alleviate the significant burden on affected women.

Ferroptosis and insulin resistance (IR) play crucial roles in the development of gestational diabetes mellitus (GDM). This study aims to analyze the effects of perillaldehyde (PAE) on ferroptosis and IR in human trophoblast cells, as well as its underlying mechanism in these effects. In this study, human trophoblasts (HTR-8/SVneo cells) treated with high glucose or in combination with insulin were used as in vitro models of GDM. The protective effects of PAE were evaluated by detecting insulin resistance and ferroptosis. GSE datasets (GSE154414 and GSE54157), SwissTargetPrediction, and GeneCards were used for gene target prediction. Results showed that PAE mitigated the decrease in HTR-8/SVneo cell viability caused by HG treatment. PAE exerted a protective effect against HG-triggered ferroptosis in HTR-8/SVneo cells by reducing ROS, Fe, and MDA levels, while increasing GSH and GPX4 levels and SOD activity. PAE alleviated IR in HTR-8/SVneo cells by increasing IRS1 and GLUT4 mRNA levels and glucose uptake, while decreasing IGF-1 mRNA level. PAE inhibited the expression of PTPN1 in HTR-8/SVneo cells with HG treatment. PTPN1 overexpression reversed the effect of PAE on ferroptosis in HTR-8/SVneo cells with HG treatment. PTPN1 overexpression counteracted the effects of PAE on IR in HTR-8/SVneo cells. PAE activated the Akt/Foxo signaling pathway by downregulating PTPN1 in HTR-8/SVneo cells under HG conditions. Akt/Foxo1 activation counteracted the effects of PTPN1 overexpression on ferroptosis and IR in HTR-8/SVneo cells with HG treatment. In conclusion, PAE attenuated IR and high glucose-triggered ferroptosis in trophoblast cells via regulation of the PTPN1/Akt/Foxo1 signaling pathway.

In the quest to enhance food production and quality of life, a variety of chemical agents that can protect crops and prevent vector borne diseases have emerged and are used indiscriminately by humans. Thus, they end up in the physiological systems through various routes. The male reproductive system is one of the highly sensitive physiological systems, despite having the blood-testis and blood-epididymis barrier. In this review, we provide a comprehensive analyses by systematically identifying specific studies that reported the relationship between endocrine disruptors and their toxicity on the male reproductive system at multiple levels. The toxicological aspects of pesticides (organophosphates, organochlorines, carbamates, pyrethroids and neonicotinoids), alkyl phenols, plasticizers, fungicides, herbicides, heavy metals, therapeutic agents, heavy metals, synthetic food preservatives, polycyclic aromatic hydrocarbons and other endocrine disrupting agents on the male reproductive system is detailed, with emphasis on the effects on endocrine signaling, HPG axis and the transgenerational toxicity. We report that endocrine disruptors can cause anatomical pathologies, destruction of specific cell types in the male reproductive organs, decreased spermatogenesis and thereby reduced sperm count, abnormality in the male gametes, altered hormonal production and transgenerational inheritance of the toxic effects.

Female genital tuberculosis (FGTB), a form of extrapulmonary tuberculosis caused by Mycobacterium tuberculosis (MTB), is an under-recognized but significant cause of female infertility, particularly in developing countries. It primarily spreads through the hematogenous route and often presents with non-specific or asymptomatic clinical features, complicating early diagnosis. Latent tuberculosis (LTB) is increasingly being identified among women with unexplained infertility and may impair reproductive outcomes by affecting ovarian reserve, endometrial receptivity, and implantation. Traditional diagnostic methods-such as smear microscopy, culture, imaging, and histopathology-suffer from low sensitivity and long turnaround times. Newer molecular techniques, including GeneXpert MTB/RIF and nucleic acid amplification test (NAAT), offer faster and more accurate detection. A comprehensive, multimodal diagnostic approach is essential for timely intervention. This review highlights the epidemiological trends, diagnostic advancements, clinical manifestations, and fertility implications of FGTB. Improved awareness and accurate detection strategies are critical for enhancing fertility outcomes in affected women.

Preeclampsia (PE), a severe pregnancy complication, arises from placental hypoxia-induced mitochondrial and endoplasmic reticulum (ER) oxidative stress, contributing to inadequate spiral artery remodeling and endothelial dysfunction. Calpastatin, a mitochondrial protective protein, mitigates oxidative stress-related pathologies, but its role in PE remains unclear. This study investigated the effects of Calpastatin on trophoblast cellular proliferation, migration, invasion, apoptosis, and the expression of autophagy protein (PINK1), mitochondrial dynamics protein (Mfn2), ER stress protein (GRP78), ATP, Ca, and mitochondrial membrane potential under hypoxia using transfected HTR8-SVneo cells. Calpastatin overexpression significantly enhanced proliferation, migration, and invasion while reducing apoptosis (P < 0.05); knockdown inversely affected these parameters under normoxic conditions. Under hypoxia, overexpression further amplified proliferation and migration (P < 0.01), whereas knockdown reduced migration at 48 h (P = 0.04) but not proliferation. Invasion decreased and apoptosis increased in both groups (P < 0.05). Calpastatin overexpression upregulated PINK1, downregulated Mfn2/GRP78, increased ATP and mitochondrial membrane potential, and reduced Ca. Conversely, knockdown suppressed Pink1/Parkin, elevated Mfn2/Drp1/GRP78, decreased ATP, and increased Ca and mitochondrial depolarization (P < 0.05). These findings demonstrate calpastatin promotes trophoblast function by maintaining mitochondrial-ER contact sites stability and ATP production, Ca homeostasis, and mitophagy mechanism, suggesting its critical role in PE pathogenesis.

This study aimed to evaluate the effect of platelet-rich plasma (PRP) on sperm motility in men with asthenozoospermia and assess its potential use in intrauterine insemination (IUI).

Recent advances in microbiome research have illuminated the complex bidirectional interactions between gut health and reproductive well-being. Understanding the gut microbiome's influence on the reproductive system and vice versa reveals how both of them can affect hormone production, immune function, and ultimately overall reproductive health. Dysbiosis, an imbalance in the gut microbial community, has been linked with a range of reproductive issues, including decreased sperm count and motility, erectile dysfunction, polycystic ovary syndrome (PCOS), endometriosis, infertility, and adverse pregnancy outcomes. This review critically evaluates emerging therapeutic interventions aimed at restoring microbial balance and enhancing reproductive health, such as use of prebiotics, probiotics, bacteriophage therapy, and fecal microbiota transplantation (FMT). By exploring the intricate interplay between gut microbiota and reproductive health, this review also emphasizes the need for integrated approaches in research and clinical practice to develop effective microbiome-based therapies for better reproductive health outcomes.