Diminished ovarian reserve (DOR) is characterized by a reduction in oocyte quantity and quality and involves complex, interconnected pathological mechanisms. This review systematically evaluates bioactive natural products, predominantly derived from Chinese herbal medicines, using a mechanism-first framework, while considering their chemical scaffolds and botanical sources as complementary descriptors. Current evidence indicates that these compounds exert ovarian-protective effects through coordinated regulation of oxidative stress, inflammatory responses, DNA-damage repair and cellular senescence, apoptosis-related signaling, ferroptosis, and autophagy-mitophagy homeostasis. Across granulosa-cell systems and animal models of chemotherapy-induced ovarian injury, irradiation, accelerated aging, and reproductive aging, representative compounds have demonstrated beneficial effects on endocrine function, follicular preservation, mitochondrial homeostasis, oocyte quality, and fertility-related outcomes. Their capacity to modulate multiple interacting pathways may be particularly valuable for DOR, given its multifactorial pathogenesis. Emerging findings further suggest that the effects of apoptosis-, autophagy-, and growth-related signaling are dependent on cell type, pathway status, dose, timing, and disease stage, highlighting restoration of ovarian homeostasis as a central therapeutic principle. Although further studies incorporating rigorous causal validation, ovarian pharmacokinetic characterization, and standardized experimental design are warranted, the available evidence supports these natural products as promising candidates for mechanistic investigation and future therapeutic development in DOR.

ObjectiveRepeated implantation failure (RIF) in in vitro fertilization-embryo transfer (IVF-ET) remains a challenging clinical issue. Although acupuncture is increasingly used as an adjunctive therapy for RIF patients, robust evidence supporting its efficacy in improving pregnancy outcomes is still lacking. This pilot study therefore aims to estimate effect sizes to inform sample size calculations for future definitive trials and to assess key feasibility parameters.Design and methodsThis single-center, two-arm, single-blind, randomized sham-controlled trial will enroll 100 women (50 per group) with RIF aged 25~40 years. Using a parallel-group design, participants will be randomized to receive either conventional Western medicine treatment combined with acupuncture (experimental group) or the same conventional Western medicine treatment combined with sham acupuncture (control group). Acupuncture or sham acupuncture will be administered twice weekly from day 5 of the menstrual cycle until the day before embryo transfer, with a minimum of three completed sessions, targeting acupoints with standardized techniques. The primary outcome will be embryo implantation rate, and secondary outcomes will include clinical pregnancy rate and serum biomarkers (β-human chorionic gonadotropin, luteinizing hormone, progesterone, and estradiol). Safety will be monitored through adverse event reporting.DiscussionThe findings of this study will provide preliminary data to guide the design of future large-scale, multicenter randomized controlled trials. Such trials would in turn generate more definitive evidence on the efficacy of acupuncture for improving pregnancy outcomes in RIF patients undergoing IVF-ET.Clinical trial registrationhttps://itmctr.ccebtcm.org.cn/, identifier ITMCTR2025000838

Diminished ovarian reserve (DOR) is a challenging obstacle impacting women' fertility globally with limited treatment option. Bushen Jianpi Tiaoxue Decoction (BJTD) has shown significant efficacy and safety in treating DOR patients, yet the molecular mechanisms behind its effect remain uncertain. Our study aimed to uncover the pharmacology and signaling pathway of BJTD in cyclophosphamide (Cy)-provoked DOR mice and 4-hydroperoxy cyclophosphamide (4-HC)-irritated KGN cells (human granulosa-like cell line) damage models. Granulosa cells from DOR patients and Cy-induced models were reanalyzed utilizing transcriptomics to predict differentially expressed genes and crucial signaling pathways. Validation experiments were conducted in vitro using KGN cells treated with 4-HC, a Cy metabolite, to establish a DOR model. Cell viability, apoptosis, oxidative stress, mitochondrial function, and ferroptosis markers were assessed using the cck8 assay, flow cytometry, fluorescence staining, RT-qPCR, and western blotting analyses. BJTD-serum was evaluated for its protective effects on 4-HC-triggered KGN damages. In vivo, a Cy-induced DOR mouse model was treated with BJTD to evaluate ovarian morphology, estrous cycle, follicle counts, hormone markers, mitochondrial apoptosis and ferroptosis levels, respectively via the vaginal smear, histological analysis, immunostaining, gene and protein expression experiments. The UPLC-MS analysis and network pharmacology were applied to identify BJTD's active ingredients, followed by molecular dockings to assess interactions with the target protein. To confirm the BJTD's mechanism of action, mTOR signaling modulation was analyzed using a specific inhibitor or activator in vitro. Transcriptomic reanalysis revealed significant gene expression differences, with LIF identified as a key target associated with apoptosis pathway. In vitro, 4-HC exposure induced apoptosis, mitochondrial dysfunction, and ferroptosis in KGN cells, accompanied by upregulation of LIF, mTOR, and FoxO3a signalings. BJTD-serum treatment significantly improved cell viability, reduced apoptosis, and alleviated oxidative stress by modulating mitochondrial function and ferroptosis markers, such as Nrf2, HO-1, and GPX4. In vivo, BJTD alleviated Cy-induced ovarian damage, improving ovarian index, estrous cycle, follicle development, and hormone levels, while reducing follicular atresia and granulosa cells apoptosis. Mechanically, BJTD suppressed Cy-induced activation of the LIF-mTOR axis and downstream mitochondrial apoptosis markers, including Cleaved Caspase 9/3, BAX, and γH2AX, while enhancing OPA1 and Bcl-2 expressions. The UPLC-MS outcome combining with network pharmacology identified mainly 20 active compounds in BJTD, with astragaloside IV exhibiting the strongest binding to the mTOR protein. The mTOR pathway modulation experiments confirmed that BJTD's protective effects are mediated through inhibition of hyperactivated mTOR phosphorylation and mitochondrial apoptosis cascades. BJTD demonstrates efficacy in alleviating Cy- and 4-HC-induced DOR models through targeting the LIF-mTOR signaling axis to suppress granulosa cells mitochondrial apoptosis and ferroptosis. These results might highlight promising therapeutic potential of BJTD for ovarian reserve preservation.

This study focuses on the impacts of polystyrene/polylactic acid microplastics (PS/PLA-MPs) on ovarian reserve and oocyte maturation in female mice, along with the underlying mechanisms. 1 μm PS-MPs and PLA-MPs were prepared, with PLA-MPs having a rougher surface and broader size distribution. In vitro, PLA-MPs showed higher cytotoxicity to granulosa cells compared to PS-MPs. In vivo, MPs exposure disrupted the estrous cycle, and damaged ovarian reserve. Granulosa cell apoptosis and cytokine activation led to transzonal projection retraction, oocyte oxidative stress, meiotic abnormalities, and reduced oocyte retrieval and polar body extrusion rate, thus reducing litter size. PS-MPs induced more severe intestinal and ovarian impairment. Analysis of feces 16S rRNA, serum metabolomics, and ovarian RNA sequencing revealed that lipoprotein lipase (LPL) was suppressed by both MPs, linking gut microbiota, lipid metabolism, and ovarian injury. Fecal microbiota transplantation as a rescue strategy in MPs exposed mice upregulated LPL, alleviating ovarian reserve decline. In PLA-MPs exposed mice, ovarian reserve related indicators partially recovered after a two-week exposure cessation. These results clarify the similarities and differences in how PS-MPs and PLA-MPs impair ovarian function via gut-ovary axis and lipid metabolism dysregulation.

Background: Uterus ageing is a crucial factor contributing to decreased fertility in older women and is also implicated in menstrual disorders, endometritis, and adenomyosis. Bushen Jianpi Tiaoxue Decoction (BJTD) is a traditional Chinese medicine formulation used to ameliorate endocrine disorders in the female reproductive system and finds extensive application in ageing-related endometrial diseases. However, the mechanisms underlying its improvement of uterus ageing have not been thoroughly investigated. Purpose: To explore the potential components and mechanisms of BJTD in ameliorating uterus ageing through network pharmacology, in vivo, and in vitro experiments. Methods: Morphological changes were observed using hematoxylin and eosin staining, collagen deposition was assessed using Masson staining, and apoptotic-related molecules were detected using Western blot. After determining the modeling doses, BJTD intervention was administered at two doses, and the expression of oxidative stress and apoptosis-related genes and proteins was measured. The levels of cellular apoptosis were evaluated using the TUNEL assay kit and Annexin V/FITC-PI assay kit. The main components of BJTD were determined by UPLC-MS, and the potential targets and mechanisms of BJTD action were explored using network pharmacology and molecular docking. BJTD-Containing Serum (BJTD-S) was extracted and applied in vitro experiments using human endometrial stroma cells (hESC) to preliminarily identify the pathways affected. Results: We demonstrated that modeling with 600 mg/kg/day D-Gal for 5 weeks significantly increased collagen deposition in uterine tissues, particularly in the glands and stroma. Additionally, it significantly elevated the levels of TNF-alpha and IL-1 beta and increased the expression of p53 and BAX while decreasing BCL-2 expression. BJTD significantly reduced the increased levels of TNF-alpha and IL-1 beta induced by D-Gal, and modulated oxidative stress markers such as SOD, MDA, GSH-Px, and T-AOC. BJTD also inhibited the cascade activation of apoptosis induced by D-Gal, suppressing the expression of cleaved-Caspase 8, cleaved-Caspase 3, and BAX. SIRT1 is a potential target of BJTD action. In vitro experiments showed that BJTD-S significantly improved D-Gal-induced apoptosis in hESC cells, and the expression levels of SIRT1, NRF2, and HO-1 were significantly decreased in D-Gal-induced hESC, and BJTD-S significantly increased their expression. Conclusion: BJTD can ameliorate oxidative stress and cell apoptosis levels in D-Gal-induced uterine aging, and its active ingredients can activate the SIRT1/NRF2 pathway to exert its effects. Importantly, our study provides novel insights into the molecular mechanisms by which traditional Chinese medicine influence uterus ageing. By specifically targeting the SIRT1/NRF2 pathway, BJTD presents a unique therapeutic approach that has not been extensively explored in previous studies, marking a significant advancement in the treatment of uterus ageing.

BACKGROUND:Ischemic stroke (IS) poses a significant public health burden in China, with high body mass index (BMI) identified as a key risk factor. Despite this, the temporal trends and sex-specific burdens of IS attributable to high BMI remain insufficiently explored. This study examines the burden of IS linked to high BMI in China from 1990 to 2021 and projects future trends to 2044. METHODS:Drawing on data from the Global Burden of Disease Study 2021, we first employed correlation analysis to examine the association between high BMI exposure and IS incidence in China over a 30-year period. Subsequently, we quantified the mortality and disability-adjusted life years (DALYs) attributable to high BMI-related IS. Our analysis included comparative assessments with global and high-income country trends, complemented by sex-stratified and age-specific evaluations. Finally, we developed forecasting models to project disease burden trajectories through 2044. RESULTS:From 1990 to 2021, China's age-standardized IS incidence initially rose before stabilizing, with males consistently exhibiting higher rates than females. High BMI exposure increased steadily and strongly correlated with IS incidence. Age-standardized mortality attributable to high BMI grew from 0.98 to 2.21 per 100,000, while DALYs more than doubled from 24.61 to 56.21 per 100,000, with males disproportionately affected. The elderly, particularly men, showed the steepest increases. Unlike global declines, China's high BMI-attributable burdens rose. Projections suggest continued growth, reaching 4.05 (male) and 3.23 (female) mortality rates by 2044, with DALYs at 101.33 and 96.63 per 100,000 respectively. CONCLUSION:High BMI contributes to a growing and sex-disparate burden of IS in China, with accelerated growth in older adults. Unlike high-income countries, China has not yet achieved declines in high BMI-attributable IS mortality and DALYs. Urgent public health interventions targeting BMI reduction, particularly in males and older populations, are needed to mitigate future burdens.

Postoperative ileus (POI) remains a prevalent and significant challenge following abdominal surgeries, precipitating patient distress, prolonged hospital stays, and escalated medical expenditures. Conventionally addressed via pharmacological interventions, POI is increasingly being explored through adjunctive therapeutic strategies, with acupuncture gaining recognition as a promising option. Acupuncture has demonstrated encouraging potential in promoting gastrointestinal motility in patients with POI. Moreover, recent research has shed light on the therapeutic mechanisms underlying its efficacy. This article aims to present a comprehensive overview of acupuncture as a treatment for POI, highlighting advancements in clinical research and recent elucidations of its mechanistic underpinnings. It aspires to contribute a pivotal reference point for scholars and enthusiasts keen on garnering a deeper understanding of acupuncture's role in managing POI.

Bushen Huatan Huoxue Formula (BHHF), a traditional Chinese medicine decoction, demonstrates potential in treating polycystic ovary syndrome (PCOS), a prevalent endocrine disorder in women of reproductive age that is closely associated with obesity and metabolic dysregulation. However, the underlying molecular mechanisms of BHHF’s action remain unclear. This study aimed to evaluate the therapeutic efficacy of BHHF in obesity-associated PCOS and investigate its regulatory mechanisms related to metabolic homeostasis. In vivo, three-week-old female Sprague Dawley rats were divided into seven groups: control, dehydroepiandrosterone (DHEA), high-fat diet (HFD), model (HFD + DHEA), low-dose BHHF, high-dose BHHF, and metformin. The PCOS model was induced by DHEA injection. BHHF was administered by gastric gavage for four weeks. Body weight, fat volume, glucose tolerance, and insulin sensitivity were measured. Ovarian histology, hormone analysis, RNA extraction, quantitative real-time PCR, protein extraction, western blotting, and proteomics studies were also conducted. In vitro, 3T3-L1 cells were used to assess lipid accumulation, mitochondrial function, and the effects of BHHF-containing serum. BHHF restored reproductive cyclicity and polycystic ovarian morphology, reduced testosterone and anti-Müllerian hormone levels, and increased estradiol levels. It also alleviated weight gain, reduced fat volume, improved glucose tolerance, and enhanced insulin sensitivity. Proteomics analysis revealed that BHHF activated the AMPK signaling pathway and promoted white adipose tissue browning. In vitro, BHHF-containing serum suppressed lipid accumulation and enhanced mitochondrial oxygen consumption. The bioactive components of BHHF–Bushen (BS), Huatan (HT), and Huoxue (HX) –exhibited specific functions. BS improved estrous cyclicity and ovarian morphology; HT regulated glucose and lipid metabolism and promoted adipose browning; and HX modulated mitochondrial bioenergetics and redox homeostasis. BHHF exerts multi-targeted therapeutic effects on obesity-associated PCOS by regulating metabolic-reproductive crosstalk. Its components act synergistically, offering a novel therapeutic strategy for PCOS treatment. Future research should focus on identifying core active compounds and optimizing treatment according to individual PCOS phenotypes.

Objective This study aims to investigate the effects of natural products on animal models of premature ovarian failure (POF). Methods We conducted comprehensive literature searches and identified relevant studies that examined the protective effects of natural products on experimental POF. We extracted quantitative data on various aspects such as follicular development, ovarian function, physical indicators, oxidative stress markers, inflammatory factors, and protein changes. The data was analyzed using random-effects meta-analyses, calculating pooled standardized mean differences and 95% confidence intervals. Heterogeneity was assessed using the I 2 statistic, and bias was estimated using the SYRCLE tool. Results Among the 879 reviewed records, 25 articles met our inclusion criteria. These findings demonstrate that treatment with different phytochemicals and marine natural products (flavonoids, phenols, peptides, and alkaloids, etc.) significantly improved various aspects of ovarian function compared to control groups. The treatment led to an increase in follicle count at different stages, elevated levels of key hormones, and a decrease in atretic follicles and hormone levels associated with POF. This therapy also reduced oxidative stress (specifically polyphenols, resveratrol) and apoptotic cell death (particularly flavonoids, chrysin) in ovarian granulosa cells, although it showed no significant impact on inflammatory responses. The certainty of evidence supporting these findings ranged from low to moderate. Conclusions Phytochemicals and marine natural product therapy (explicitly flavonoids, phenols, peptides, and alkaloids) has shown potential in enhancing folliculogenesis and improving ovarian function in animal models of POF. These findings provide promising strategies to protect ovarian reserve and reproductive health. Targeting oxidative stress and apoptosis pathways may be the underlying mechanism.

Background Polycystic ovary syndrome (PCOS) is a common endocrine and metabolic disorder in premenopausal women, often linked to abdominal obesity, insulin resistance, and metabolic issues. With its heterogeneous nature, PCOS treatment should be tailored to individual symptoms and patient preferences. This study examines collaboration networks among countries, institutions, authors, references, and journals related to PCOS treatment.Methods Web of Science data was analyzed using VOSviewer and CiteSpace for bibliometric visualization. Chinese and Western medicine treatments for PCOS were reviewed, emphasizing symptom-targeted solutions.Results Data from 4682 records authored by 400 individuals from 515 institutes in 62 countries revealed China as the leading contributor. Notable authors include Monash University and Richard S. Legro. Common research themes include adipocytes, inflammation, insulin sensitivity, oxidative stress, and the gut microbiome. Tailoring treatment to individual needs is essential, focusing on hyperandrogenism, ovulation, and insulin resistance, with lifestyle counseling to address obesity.Conclusion This bibliometric analysis provides valuable insights into the research status of PCOS treatment. China has made significant contributions, and complementary and alternative therapies, such as traditional Chinese medicine and acupuncture, have also shown beneficial effects recently. The research on inflammation, oxidative stress, and the gut microbiome may provide new targets and strategies for the treatment of PCOS. The recognition of the metabolic problems in PCOS patients facilitates the formulation of more personalized treatment plans to improve the prognosis of patients.

Mesenchymal stem cells (MSCs) are a prevalent source for stem cell therapy and play a crucial role in modulating both innate and adaptive immune responses. Non-alcoholic fatty liver disease (NAFLD) is characterized by the accumulation of triglycerides in liver cells and involves immune system activation, leading to histological changes, tissue damage, and clinical symptoms. A recent publication by Jiang et al , highlighted the potential of MSCs to mitigate in NAFLD progression by targeting various molecular pathways, including glycolipid metabolism, inflammation, oxidative stress, endoplasmic reticulum stress, and fibrosis. In this editorial, we comment on their research and discuss the efficacy of MSC therapy in treating NAFLD.

Background Semen Cuscutae and Fructus Lycii (SC-FL) is known for its potential therapeutic effects on spermatogenesis dysfunction. However, the underlying mechanisms of SC-FL in alleviating spermatogenesis dysfunction is still being elucidated. Purpose This study aimed to explore the effects of SC-FL on spermatogenesis dysfunction and investigate the involved mechanisms, specifically focusing on the modulation of oxidative stress and ferroptosis. Methods A mouse model of spermatogenesis dysfunction was induced by tripterygium glycosides, followed by treatment with SC-FL. Assessment of testicular spermatogenic function in the mice was performed alongside lipidomics analysis to investigate the metabolic mechanisms of SC-FL. The effects on oxidative stress and ferroptosis-related markers were evaluated, the chemical constituents of SC-FL were identified using liquid chromatography-mass spectrometry, and network pharmacology analysis was carried out. Additionally, an in vitro model of spermatogenesis dysfunction was established using triptolide-induced GC-1 cells, which were treated with Lycium barbarum polysaccharides (LBP) and flavonoids from Semen Cuscutae (FSC) to explore their impact on cell damage, oxidative stress-mediated damage, and ferroptosis. Results SC-FL improved the mouse model of spermatogenesis dysfunction by inhibiting oxidative stress-mediated ferroptosis. In vitro experiments demonstrated that LBP and FSC relieved GC-1 cell damage, with their mechanisms also associated with the inhibition of oxidative stress-mediated ferroptosis. Conclusion SC-FL alleviates spermatogenesis dysfunction in animal and cell models, potentially through the modulation of the Nrf2/HO-1 signaling pathway, which consequently inhibits oxidative stress-mediated ferroptosis in spermatogonial cells.

ObjectiveTo comprehensively assess the global, regional and national burden of polycystic ovary syndrome (PCOS) in incidence, prevalence, and years lived with disability (DLYs) based on the Global Burden of Disease Study (GBD) 2019.MethodsThis was a cross-sectional descriptive study. Data on PCOS incidence, prevalence, and DLYs from 1990 to 2019 were obtained from the GBD study 2019. According to the commonwealth income, WHO region, and the sociodemographic index, the estimates were demonstrated along with the estimated annual percentage change (EAPC). The EAPC data were analyzed by four levels of hierarchical clustering and displayed in the world map. The Autoregressive Integrated Moving Average (ARIMA) and Bayesian age-period-cohort (BAPC) model was used to predict the PCOS burden in the next 20 years.ResultsFrom 1990 to 2019, the number of PCOS incidence in one year increased from 1.4 million in 1990 to 2.1 million in 2019 (54.3%). Only the EAPC estimates of incidence in the Region of the Americas decreased, and their aged-standardized incidence rate (ASIR) values were the highest in 1990 and 2019. There was no significant correlation between human development index (HDI) and EAPC. However, when HDI < 0.7, EAPC of incidence and prevalence was positively correlated with HDI, and when HDI > 0.7, EAPC of incidence and prevalence was negatively correlated with HDI. Countries with the middle level HDI have the highest increasing trend of ASIR and age-standardized prevalence rate (ASPR). The 10 to 19 years old group had the highest incidence counts of PCOS globally. Besides, the ARIMA and BAPC model showed the consistent increasing trend of the burden of PCOS.ConclusionIn order to better promote the early diagnosis and treatment, expert consensus and diagnosis criteria should be formulated according to the characteristics of different ethnic groups or regions. It is necessary to emphasize the early screening and actively develop targeted drugs for PCOS.

Bushen Tiaoxue Granules (BTG) is an empirical Chinese herbal formula that has been used for the treatment of subfertility. The protective effect of BTG on controlled ovarian hyperstimulation (COH)-induced impaired endometrial receptivity has been reported in our previous study. This study aims to explore the mechanisms of BTG on ameliorating abnormal morphology of endometrium based on network pharmacology. Active compounds of BTG were identified via the traditional Chinese medicine systems pharmacology and UPLC-MS technology. The SwissTargetPrediction platform and HERB database were used to screen out the putative targets of BTG. Potential targets of endometrial dysfunction caused by COH were obtained from three GEO databases. Through the STRING database, the protein–protein interaction was carried out according to the cross-common targets of diseases and drugs. GO terms and KEGG pathways enrichment analyses were conducted via the Metascape database. AutoDock Vina was used for docking validation of the affinity between active compounds and potential targets. Finally, in vivo experiments were used to verify the potential mechanisms derived from network pharmacology study. A total of 141 effective ingredients were obtained from TCMSP and nine of which were verified in UPLC-MS. Six genes were selected through the intersection of 534 disease related genes and 165 drug potential targets. Enrichment analyses showed that BTG might reverse endometrial dysfunction by regulating adherens junction and arachidonic acid metabolism. Hematoxylin–eosin staining revealed that BTG ameliorated the loose and edematous status of endometrial epithelium caused by COH. The protein expression of FOXO1A, β-Catenin and COX-2 was decreased in the COH group, and was up-regulated by BTG. BTG significantly alleviates the edema of endometrial epithelium caused by COH. The mechanisms may be related to adheren junctions and activation of arachidonic acid metabolism. The potential active compounds quercetin, taxifolin, kaempferol, eriodictyol, and isorhamnetin identified from the BTG exhibit marginal cytotoxicity. Both high and low concentrations of kaempferol, eriodictyol, and taxifolin are capable of effectively ameliorating impaired hESC cellular activity.

BackgroundStroke is a devastating global health issue, with high mortality and disability rates. The increasing prevalence of male infertility among reproductive-aged men has become a growing concern worldwide. However, the relationship between male infertility and stroke incidence remains uncertain. This study aimed to address this knowledge gap by employing a Mendelian randomization (MR) approach.MethodUtilizing genetic instrumental variables derived from a genome-wide association study (GWAS) on male infertility and stroke, a two-sample MR design was implemented. Five different analysis methods, with inverse-variance weighted as the primary approach, were used to examine the genetic causal associations between male infertility and various stroke subtypes. Heterogeneity analysis, pleiotropy tests, and leave-one-out validation were conducted to assess heterogeneity, evaluate pleiotropy, and ensure the robustness of the findings.ResultThe results indicate a potential lower risk of small vessel stroke associated with male infertility (odds ratio, 95% confidence interval: 0.82, 0.68 to 0.99, p=0.044), although no significant impact on other stroke subtypes was observed. The study exhibited low heterogeneity and no apparent pleiotropy; however, the stability of the results was not optimal.ConclusionMale infertility might potentially confer a protective effect against small vessel stroke risk. Caution is warranted due to potential confounding factors. Additional studies are necessary to confirm these findings and provide further validation.

The incidence of premature ovarian insufficiency (POI) is increasing worldwide, particularly among younger women, posing a significant challenge to fertility. In addition to menopausal symptoms, POI leads to several complications that profoundly affect female reproductive function and overall health. Unfortunately, current clinical treatment strategies for this condition are limited and often yield unsatisfactory outcomes. These approaches typically involve hormone replacement therapy combined with psychological support. Recently, mesenchymal stem cell (MSC) therapies for POI have garnered considerable attention in global research. MSCs can restore ovarian reproductive and endocrine functions through diverse mechanisms, including controlling differentiation, promoting angiogenesis, regulating ovarian fibrosis, inhibiting apoptosis, enhancing autocrine and paracrine effects, suppressing inflammation, modulating the immune system, and genetic regulation. This editorial offers a succinct summary of the application of MSC therapy in the context of POI, providing evidence for groundbreaking medical approaches that have potential to enhance reproductive health and overall well-being for women.

Endometrial receptivity is affected by many physiological and pathological factors, and the mechanism is complex, which is difficult to fully explain. Establishment of appropriate animal models is a necessary condition for exploring the mechanism of poor endometrial receptivity and drug research. At present, there is no review to evaluate the models. In this paper, the recognized models at home and abroad are summarized, taking old age, obesity, thin uterus and endometriosis as the non-drug intervention models, and ovarian hyperstimulation, polycystic ovary syndrome, adenomyosis and drug abortion as the drug intervention models. At the same time, the gene editing and disease syndrome combination models are introduced, the effects of the models on different indicators are compared, and the advantages and disadvantages of modeling are analyzed to provide reference for future research.

随着生活和社会环境的改变及生活工作压力的增加,我国男性生育能力显著下降,男性不育症发病率逐年增高,给男科医生带来了前所未有的挑战和治疗难题.中医药治疗男性不育症具有明确疗效,临床上应用广泛,为了明确中医药在男性不育症的不同种类及不同阶段做起的作用,中华中医药学会组织邀请了男科临床一线的西医与中医青年优秀专家,围绕特发性少、弱、畸形精子症、精液液化异常、精索静脉曲张、免疫性不育、提高辅助生殖技术成功率、改善抑郁焦虑状态等6个方面进行了讨论.就中医治疗的优点、特色、短板及优势病种、优势环节进行了深入探讨,针对男性不育症的各种病因及相关环节的治疗进行了梳理与归纳.男性不育症由于病因不完全明确及发病机制复杂等原因,单纯西医治疗不能达到较好的疗效,而中医药以整体观为核心,改善功能性疾病是学科优势,同时可以对应多靶点、多病因,并且有内治外治等综合性疗法,因此中医治疗及中西医医结合治疗男性不育症,在临床上应用广泛.该文总结了纯中医治疗及中西医结合治疗的优势病种和优势环节,罗列了相关病种的中西医治疗建议,以期让更多男科医生了解中医的治疗效应及优势能够实现中西借鉴、沟通融合,在临床实际诊疗中给患者提供优效、个性化的治疗方案,从而提高男性不育症的疗效.