Alzheimer's disease (AD), a leading cause of dementia, remains incurable, necessitating novel insights into its pathogenesis and therapeutic strategies. Recent studies highlight cuproptosis-a copper (Cu)-dependent mitochondrial cell death pathway-as a critical player in AD progression. Cuproptosis is triggered by Cu overload, which disrupts mitochondrial tricarboxylic acid cycle enzymes, resulting in toxic aggregation of lipoylated proteins and iron-sulfur cluster destabilization. This process exacerbates mitochondrial dysfunction, oxidative stress, and neuronal loss, synergizing with hallmark AD pathologies like Aβ deposition and Tau hyperphosphorylation. Unlike ferroptosis or apoptosis, cuproptosis uniquely involves mitochondrial protein lipoylation and Cu homeostasis imbalance. Therapeutic strategies targeting cuproptosis include Cu chelators, inhibitors of Cu transporters, antioxidants, and gene editing approaches to restore Cu homeostasis or mitigate protein aggregation. Immunotherapy and neuroprotective agents further show promise in alleviating cuproptosis-driven neuroinflammation. Despite preclinical advancements, challenges remain in balancing Cu's essential roles with therapeutic interventions. This review underscores cuproptosis as a pivotal mechanism in AD and outlines emerging therapeutic avenues, emphasizing the ncessity for precision in targeting Cu dysregulation to halt neurodegeneration.

Polycystic ovary syndrome (PCOS) is a highly prevalent endocrine and metabolic disease. This study aimed to investigate the synergistic role of immune dysregulation and ferroptosis during the pathogenesis of PCOS. Through integrating multiple Gene Expression Omnibus (GEO) datasets, differentially expressed genes (DEGs) were screened and subjected to functional enrichment analysis; weighted gene co‑expression network analysis combined with LASSO, RandomForest, and support vector machine‑recursive feature elimination algorithms were employed to identify key candidate genes; in vitro, human ovarian granulosa cells (KGN) were treated with dihydrotestosterone (DHT), NNMT expression was regulated via lentiviral vectors together with ferroptosis inhibitor intervention, and cell viability, cytotoxicity, and ferroptosis‑related indicators were examined; in vivo, a PCOS mouse model was established using dehydroepiandrosterone, and ovarian pathology, hormone levels, as well as molecular expression of the ferroptosis pathway were analyzed. DEGs in PCOS were significantly enriched in immune response and ferroptosis pathways. Twelve candidate genes were identified through screening multiple GEO datasets and demonstrated diagnostic potential. DHT induced ferroptosis in KGN cells by upregulating NNMT, manifesting as reduced cell viability, increased LDH release, accompanied by Fe²⁺ accumulation, enhanced lipid peroxidation, downregulation of SLC7A11/GPX4, and upregulation of ACSL4. This process could be partially reversed by ferroptosis inhibitors. Knockdown of NNMT effectively alleviated the DHT‑induced ferroptosis phenotype. Ovaries from PCOS mice exhibited typical pathological alterations, concurrent with elevated NNMT expression and abnormal activation of the ferroptosis pathway. This study has uncovered novel mechanisms underlying the development and progression of PCOS, offering potential targets for its diagnosis and treatment.

Ischemic stroke (IS) is characterized by high rates of morbidity, disability and mortality. The pathological process underlying IS involves spatiotemporal dynamic responses of multiple cell types and marked cellular heterogeneity which cannot be fully elucidated using traditional bulk sequencing technologies. Single-cell RNA sequencing (scRNA-seq) and spatial transcriptomics (ST) have provided high-resolution tools for investigating pathological mechanisms and developing precise diagnostic and therapeutic strategies for IS. In this review, we systematically summarize the core principles, mainstream platform characteristics and applicability of these two technologies in IS research, focusing particularly on how they have helped to reveal dynamic cellular evolution following ischemia, spatial molecular heterogeneity between the infarct core and penumbra, and key differences between human and mouse models. We also review key breakthroughs, including the LGALS9-CD44 repair signaling axis, the optimization of oligodendrocyte precursor cell (OPC) transplantation, and the molecular classification of IS. In addition, we discuss the potential for this technology to be translated clinically, and analyze the levels of accompanying evidence for relevant research findings from four dimensions: the screening of early diagnostic biomarkers, the development of novel therapeutic targets, improving molecular understanding for cell therapy, and the construction of disease classifications at the molecular level. We also highlight potential core challenges including the low capture efficiency of brain cells, inherent contradiction between spatial resolution and sensitivity, scarcity and insufficient standardization of human samples, and prominent obstacles in translating preclinical results to clinical practice. In future, the optimization of technologies that are specific to brain tissue, the construction of multicenter large-sample human stroke databases, and the implementation of cross-species validation studies, will help to promote the application of scRNA-seq and ST from basic mechanistic analysis to precise clinical application in the field of IS, thereby providing scientific support for improving the diagnosis and treatment of IS.

Background:Previous Mendelian randomization (MR) studies explored causal links between polycystic ovary syndrome (PCOS) and pregnancy complications and adverse outcomes mainly in European populations, with limited generalizability. This two-sample MR study addresses this limitation. Methods:Independent genetic instruments for PCOS were selected at genome-wide significance (P<5×10-8) and statistical pruned using LDTrait. East Asian (EAS)-based genome-wide association study data were analyzed for gestational diabetes mellitus (GDM), preeclampsia, intrahepatic cholestasis of pregnancy, miscarriage, preterm birth, and gestational age at birth. The inverse variance-weighted (IVW) method with Bonferroni correction served as the primary analysis, supplemented by pleiotropy and heterogeneity tests. Multivariable MR (MVMR) assessed direct effects by adjusting for confounders. Results:Genetically predicted PCOS was causally linked to increased GDM risk (OR=1.203, 95% CI: 1.00-1.433), with consistent evidence across debiased IVW (OR=1.207, 95% CI: 1.008-1.444), Bayesian Weighted MR (OR=1.204, 95% CI: 1.007-1.440), Contamination Mixture (OR=1.231, 95% CI: 1.141-1.526), and distortion test (OR=1.203, 95% CI: 1.120-1.291). The strongest single nucleotide polymorphisms (SNP)-level effect was observed for rs1894116 (YAP1), followed by rs2268361 (FSHR). MVMR confirmed independence from body mass index (BMI), though the effect disappeared after adjusting for glucose and lipid traits. No causal relationships were found between PCOS and other outcomes (P>0.05). Conclusion:This MR study provides evidence supporting a potential causal association between genetically predicted PCOS and GDM in East Asian populations, in contrast to previous European-based findings, and highlights possible population-specific genetic differences with implications for precision risk assessment in pregnancy.

Diabetes and its complications are a major global public health issue. Conventional Western medicine has limitations in efficacy and safety in managing complications, while acupuncture, with multitarget regulation and low side effects, serves as an important supplementary therapy. This review discusses how acupuncture relieves macrovascular complications, such as angina and cerebral reperfusion, by inhibiting NF-κB, improving vascular endothelial function, and regulating autonomic nerves. In addition, acupuncture delays microvascular complications, such as retinopathy and proteinuria via vasodilation, anti-inflammatory effects, antioxidative effects, and neurotrophic promotion. Acupuncture also benefits other complications by enhancing microcirculation and neuroendocrine function. The mechanisms of acupuncture involve regulating the metabolic-inflammatory-neurovascular network, activating pathways (such as GLP-1 and SDF-1), and repairing cellular structures. Modern technologies—including artificial intelligence (AI) for individualized acupoint selection, functional magnetic resonance imaging (fMRI) for central regulation visualization, and biomaterial combination for diabetic foot repair—enhance the precision of acupuncture. However, clinical translation of acupuncture faces the following challenges: fragmented mechanisms; insufficient clinical evidence, including small samples, short follow-ups, and a lack of long-term safety data when used with new hypoglycemics; and technical nonstandardization, such as inconsistent acupoint selection, nonuniform operation parameters, and poor adaptability of AI to traditional Chinese medicine syndrome differentiation. Future research should deepen the exploration of the neuroendocrine–immune network via interdisciplinary integration, conducting large-sample long-term trials, establishing standardized protocols, and validating AI/fMRI-assisted precision acupoint selection to accelerate the transition of acupuncture from adjuvant to precision therapy to improve patients’ quality of life.

This study aimed to investigate the neuroprotective effects of electroacupuncture (EA) at the Baihui and Dazhui acupoints in a rat model of ischemia-reperfusion injury. Ninety-six male Sprague–Dawley rats were randomly assigned to four groups ( n = 24 per group): Sham, middle cerebral artery occlusion (MCAO), MCAO+EA, and MCAO+MCC950. The MCAO model was induced using filament embolization. Neurological function was assessed using Zea Longa scores on days 1 and 7 posttreatment, while cerebral infarction volume was measured using 2,3,5-triphenyltetrazolium chloride staining. Gene expression levels of NLRP3 and GSDMD were quantified by RT-qPCR, and protein expressions of NLRP3, GSDMD, caspase-1, IL-1β, and IL-18 were evaluated via Western blotting, immunohistochemistry, immunofluorescence staining, and ELISA. On day 1, compared with the MCAO group, the MCAO+EA and MCAO+MCC950 groups exhibited significantly reduced mRNA and protein expressions of NLRP3 and GSDMD ( P < 0.05), as well as decreased levels of caspase-1, IL-1β, and IL-18 ( P < 0.05). However, no significant differences were observed in neurological deficit scores or cerebral infarction volume. By day 7, both the MCAO+EA and MCAO+MCC950 groups showed significant improvements in neurological function ( P < 0.05), reductions in cerebral infarction volume ( P < 0.05), and further decreases in the expression of NLRP3, GSDMD, caspase-1, IL-1β, and IL-18 ( P < 0.05). EA at the Baihui and Dazhui acupoints alleviates neurological deficits in ischemic stroke rats by inhibiting the NLRP3/caspase-1 inflammatory pathway and reducing the expression of apoptosis-related proteins such as NLRP3, GSDMD, caspase-1, IL-1β, and IL-18.

Numerous research conducted in recent years has revealed that gut microbial dysbiosis, such as modifications in composition and activity, might influence lung tissue homeostasis through specific pathways, thereby promoting susceptibility to lung diseases. The development and progression of lung cancer, as well as the effectiveness of immunotherapy are closely associated with gut flora and metabolites, which influence immunological and inflammatory responses. During abnormal proliferation, non-small cell lung cancer cells acquire more substances and energy by altering their own metabolic pathways. Glucose and amino acid metabolism reprogramming provide tumor cells with abundant ATP, carbon, and nitrogen sources, respectively, providing optimal conditions for tumor cell proliferation, invasion, and immune escape. This article reviews the relationship of immune response with gut flora and metabolic reprogramming in non-small cell lung cancer, and discusses the potential mechanisms by which gut flora and metabolic reprogramming affect the occurrence, development, and immunotherapy of non-small cell lung cancer, in order to provide new ideas for precision treatment of lung cancer patients.

Ischemic stroke (IS) has high morbidity/mortality with limited treatments. This study screened core copper homeostasis-related genes in IS and validated their function as precise intervention targets. Human IS gene chip data were retrieved from GEO, and copper homeostasis genes from multiple databases. After data correction/normalization, IS differentially expressed genes (DEGs) were identified and intersected with copper genes. DAVID for GO/KEGG enrichment, STRING for PPI network, CytoHubba for key genes, and ROC curves for diagnostic value. MCAO rat models were established; after 14-day rearing, protein expression was validated via relevant assays. 1,425 IS DEGs and 2,610 copper genes intersected to 235 genes, enriched in inflammatory response, innate immunity, and TNF/NOD-like/Toll-like receptor pathways. Key genes HIF-1α, TNF, TLR4, IL-1β had IS diagnostic AUC 0.70–0.80. MCAO rats showed worse neurological deficits, larger infarcts, neuronal damage, brain copper accumulation, and upregulated key genes linked to neuroinflammation, BBB disruption, and neuronal injury. Bioinformatics and animal studies revealed copper homeostasis imbalance-related genes mediate inflammation, oxidative stress, and mitochondrial regulation, supporting the "copper accumulation–inflammation–oxidative stress" cascade. These genes may be novel IS targets. Further study on dynamic expression across ischemic time windows/brain regions and interactions with other cell death modes is needed. This study used a system approach: bioinformatics screening → experimental validation → mechanism elucidation. Three cerebral ischemia datasets from GEO (GSE16561, GSE22255, GSE58294) underwent DEG analysis; Venn diagram identified core shared DEGs. GO/KEGG enrichment, STRING for PPI network, Cytoscape for hub genes, ROC curves for diagnostic potential. Rat MCAO model was established; validity verified via relevant staining; Cu2+ accumulation detected; molecular expression validated by assays.

BackgroundLow back pain (LBP) is one of the most common symptoms of osteoporosis (OP), but LBP caused by osteoporosis can easily be masked by other causes, leading to misdiagnosis. However, there are currently no convenient tools available to identify patients with low back pain caused by osteoporosis.MethodsWe consecutively enrolled 769 patients diagnosed with low back pain in our hospital from January 2019 to March 2024. A total of 355 cases were excluded due to relevant missing data, leaving a final analysis cohort of 414 cases. The dataset was randomly divided into a training group and a validation group at a ratio of 7:3 for further analysis. in this preliminary analysis were selected for subsequent multivariate analysis. Least absolute shrinkage and selection operator(LASSO) was employed to identify the associated risk factors for osteoporosis. Independent variables with P<0.05 in univariate analysis were included in the multivariate analysis to construct the prediction model. Once the regression equation was established, a nomogram was utilized to visualize the prediction model, while receiver operating characteristic (ROC) curve was plotted to evaluate its performance, specifically by calculating the area under the curve (AUC) which represents discrimination ability of the model. To assess goodness-of-fit, calibration curve was generated for evaluating calibration accuracy. Furthermore, decision curve analysis (DCA) served to determine clinical application value of this predictive model. Statistical significance level was set at P < 0.05.ResultsBuilding upon the LASSO and multivariate Cox regression, eleven variables were significantly associated with OP (i.e., gender, age, history of fracture, history of alcohol consumption, history of rheumatoid arthritis, hematocrit, red blood cell volume distribution width, lymphocyte percentage, triglyceride, potassium ion, and alanine aminotransferase). In training and validation sets, AUCs and C-indexes of the OP prediction models were all greater than 0.8(AUC: 0.914 for training; 0.833 for validation), which indicated excellent predictability of models. On the whole, the calibration curves coincided with the diagonal in two models. DCA indicated that the models had higher clinical benefit than other risk factors. While confirmed the clinical utility of the model, as it outperformed both the ‘treat-all’ and ‘treat-none’ strategies.ConclusionAfter verification, our prediction models of OP are reliable and can predict the incidence of osteoporosis, providing valuable guidance for clinical prognosis estimation and individualized administration of patients with LBP(a new way for early identification and intervention of patients with osteoporosis).

To clarify the specific mechanism underlying the effect of running in a plateau hypoxic environment (PHE) on autonomic nervous system (ANS) function, address the limitations of existing single-dimensional and interdisciplinary research in current studies, and provide new insights into the regulatory role of ANS in plateau adaptation. A comprehensive review was conducted across five dimensions: an overview of ANS physiology; the physiological effects of PHE on the human body; specific mechanisms by which running under PHE modulates ANS function; comparative analysis of running in PHE versus other training modalities; and prospects for future research. Running in PHEs triggers a continuous ANS response, transitioning from mild activation under moderate intensity or altitude, to acute sympathetic dominance at higher intensities or altitudes, and finally to parasympathetic rebalancing during chronic exposure or training. This adaptive process enhances cardiopulmonary function, optimizes oxygen transport efficiency, and increases lactate tolerance, thereby improving aerobic metabolic capacity, hypoxia tolerance, and running economy in athletes. Compared with high-intensity hypoxic–low-altitude training and intermittent hypoxic training, running in PHEs offers unique advantages in maximizing physiological potential, though its application is constrained due to geographical accessibility. The ANS plays a central regulatory role in human adaptation to running in PHEs. This study systematically clarifies the adaptive mechanisms and athletic performance-enhancing effects of such exercise, establishes a theoretical foundation for subsequent research on plateau training and ANS regulation, and highlights directions for developing personalized training programs and advancing technological innovation.

Polycystic ovary syndrome (PCOS) is a common gynaecological endocrine disorder that affects women of reproductive age and is often accompanied by clinical symptoms such as acne, obesity, menstrual disorders, and ovulation disorders. Although the molecular mechanisms underlying the pathophysiology of PCOS are still unknown despite the condition’s extremely complex underlying mechanism, recent studies suggest that glycolysis may be involved in PCOS pathogenesis, including hyperandrogenism, inflammation, ovulatory dysfunction, and diminished endometrial receptivity and infertility. Therefore, there is an urgent need to explore the pathogenesis and treatment of glycolysis in patients with PCOS. The present review discusses the mechanism of glycolysis, the association between glycolysis and diverse features of PCOS, the molecular mechanism underlying the involvement of glycolysis in the pathogenesis of PCOS, and some common treatment strategies involving glycolysis in patients with PCOS. More prospective studies using advanced detection technologies such as Seahorse are needed to elucidate the specific molecular mechanisms through which glycolysis is involved in the pathogenesis of PCOS.

BACKGROUND:Chemotherapy-induced immunosuppression significantly impacts patient's quality of life. Umbelliferone (UMB) is known for its anti-inflammatory, antioxidant, and anti-apoptotic properties, but its effects on cyclophosphamide (CTX)-induced immunosuppression need further study. METHODS:We established a CTX-induced immunosuppressed mouse model and administered varying doses of UMB. Immune function was assessed by evaluating white blood cells, lymphocytes, thymus and spleen indices, and CD4+/CD8+ T cell ratios. Serum levels of IL-2, IFN-γ, IgA, IgM, and IgG, along with macrophage phagocytic activity, NK cytotoxicity, and lymphocyte proliferation, were measured. Untargeted metabolomics was used to identify key pathways regulated by UMB, and RT-qPCR and Western blotting were performed to analyze the expression of related enzymes and metabolites. RESULTS:UMB intervention increased white blood cells, lymphocytes, thymus and spleen indices, and CD4+/CD8+ T cell ratios in CTX-immunosuppressed mice. It reversed reduced levels of serum IL-2, IFN-γ, IgA, IgM, and IgG and improved macrophage phagocytic activity, NK cytotoxicity, and lymphocyte proliferation. Key pathways identified by metabolomics included histidine and purine metabolism. UMB improved levels of histamine, L-glutamate, L-aspartate, xanthine, dAMP, deoxyinosine, xanthosine, and cGMP and upregulated HDC, ASPA, and PNP while downregulating XDH, PDE5, ROS, and MDA in spleen tissue. UMB enhanced SOD activity and GSH levels and reduced apoptosis, as indicated by lower TUNEL-positive expression. CONCLUSION:UMB enhanced immune function in CTX-immunosuppressed mice through the regulation of histidine and purine metabolism, exhibiting antioxidant and anti-apoptotic effects. These findings highlight the potential of UMB in mitigating immunosuppression.

An extensive network of cutaneous nerves, neuropeptides, and specific receptors richly innervates the skin and influences a variety of physiological and pathological processes. The sensory and autonomic nerve fibers secrete a variety of neuropeptides that are essential to the different phases of wound healing. In addition to initiating a neurogenic inflammatory response in the early stages of healing, neuropeptides also control wound healing by influencing immune cells, repair cells, and the growth factor network. However, the precise mechanism by which they accomplish these roles in the context of cutaneous wound healing is still unknown. Investigating the mechanisms of action of neuropeptides in wound healing and potential therapeutic applications is therefore urgently necessary. The present review discusses the process of wound healing, types of neuropeptides, potential mechanisms underlying the role of neuropeptides in cutaneous wound healing, as well as some neuropeptide-derived treatment strategies, such as hydrogels, new dressings, electro stimulation, and skin-derived precursors. Future in-depth mechanistic studies of neuropeptides in cutaneous wound healing may provide opportunities to develop therapeutic technologies that harness the roles of neuropeptides in the wound healing process.

Polycystic ovary syndrome (PCOS) is the predominant endocrine disorder among women of reproductive age and represents the leading cause of anovulatory infertility, which imposes a considerable health and economic burden. Currently, medications used to treat PCOS can lead to certain adverse reactions, such as affecting fertility and increasing the risk of venous thrombosis. Drug delivery systems utilizing nanomaterials, characterized by prolonged half-life, precision-targeted delivery, enhanced bioavailability, and reduced toxicity, are currently being employed in the management of PCOS. This innovative approach is gaining traction as a favored strategy for augmenting the therapeutic efficacy of medications. Consequently, this paper discusses the roles of nanoparticles, nanocarriers, and targeted ligands within nanomaterial-based drug delivery systems, aiming to identify optimal methodologies for treating PCOS using nanomaterials. Additionally, prospective research avenues concerning nanomaterial-based delivery systems in the context of PCOS, as well as the implications of existing insights on the advancement of novel therapies for PCOS, are highlighted.

ObjectiveTo evaluate the effectiveness of different acupuncture treatments for mammary gland hyperplasia (MGH) using a network meta-analysis.MethodsSeveral databases were searched without language restrictions from 2000 to February 2023, including PubMed, Embase, Web of Science, Cochrane Library, China Science and Technology Journal Database, China Biology Medicine Database, Wanfang Database, China National Knowledge Infrastructure Database, and other professional websites and gray literature. Inclusion criteria were adult women diagnosed with MGH; intervention measures included acupuncture and related therapies; the control group was treated with simple drugs; and the research type was a randomized controlled trial (RCT). The primary outcomes were treatment effectiveness and estradiol and progesterone levels. Secondary outcomes were breast lump size and visual analog scale (VAS) score of breast pain. Exclusion criteria were studies unrelated to MGH, incorrect study populations, control measures or interventions, incomplete data, non-RCTs, case reports, and animal experiments. Cochrane tools were used to assess the risk of bias. The R software (x64 version 4.2.1), Review Manager 5.3 software and STATA 16.0 software were used for data analysis.ResultsFollowing a rigorous screening process, data extraction, and quality assessment, 48 eligible RCTs encompassing 4,500 patients with MGH and 16 interventions were included. The results indicated that acupuncture, alone or in combination with traditional Chinese or Western medicine, had better therapeutic effects than conventional therapy. In terms of effectiveness, warm needle acupuncture was the best choice (94.6%). Bloodletting pricking was the most effective method (85.7%) for lowering progesterone levels. Bloodletting pricking was the most effective method (98.3%) for lowering estradiol levels. Manual acupuncture combined with traditional Chinese medicine was the most effective (74.5%) treatment to improve the size of the breast lump. Warm needle acupuncture was the most effective (69.8%) in improving the VAS score.ConclusionAcupuncture therapy was more effective in treating MGH than drug therapy alone, and warm needle acupuncture and bloodletting pricking were the two best options. However, larger sample sizes and high-quality RCTs are required.

The present study centers on the impact of Acupuncture on enhancing blood circulation in adenomyosis and its underlying mechanisms. The progression of adenomyosis is intricately linked to factors such as vascular tone, blood flow rate, and platelet aggregation. The paper delves into the mechanisms through which Acupuncture facilitates the improvement of blood circulation. A thorough review of pertinent literature reveals that Acupuncture can effectively enhance blood circulation via diverse mechanisms, thereby exerting a beneficial influence on adenomyosis.

Annually, more than 15 million people worldwide suffer from stroke, a condition linked to high mortality and disability rates. This disease significantly affects daily life, impairing everyday functioning, executive function, and cognition. Moreover, stroke severely restricts patients’ ability to perform daily activities, diminishing their overall quality of life. Recent scientific studies have identified cuproptosis, a newly discovered form of cell death, as a key factor in stroke development. However, the role of cuproptosis in stroke remains unclear to researchers. Therefore, it is crucial to investigate the mechanisms of cuproptosis in stroke’s pathogenesis. This review examines the physiological role of copper, the characteristics and mechanisms of cuproptosis, the differences and similarities between cuproptosis and other cell death types, and the pathophysiology of cuproptosis in stroke, focusing on mitochondrial dysfunction and immune infiltration. Further research is necessary to understand the relationship between previous strokes and cuproptosis and to clarify the mechanisms behind these associations.

Abstract Objective:To investigate the neuroprotective effects of electroacupuncture at Baihui and Dazhui on rats in an ischemia-reperfusion injury model. Methods: Forty-eight SPF male SD rats were randomly divided into sham operation group, model group, EA group and inhibitor group, with 12 rats in each group, and the middle cerebral arteryOcclusion (MCAO) model was established using the wire embolization method, and the model was successfully replicated and treated by acupuncture at Baihui and Dazhui. The neurological function scores were evaluated by Zea Longa neurological deficit score on days 1, 7 and 14 after treatment, and the volume of cerebral infarction was measured by 2, 3, 5-triphenyltetrazolium chloride staining. Detection of nod-like receptor protein 3 (NLRP3) and GSDMD gene expression by real-time fluorescence quantitative PCR , Western blot detection of NLRP3, GSDMD, Caspase-1 and other protein expression levels in rat brain tissue , and microglia levels were observed by immunofluorescence staining; the expression levels of interleukin-1β (IL-1β) and interleukin-18 (IL-18) were detected by enzyme-linked adsorption assay. Results:Compared with the model group, the rats in the electroacupuncture group had significantly lower neurological deficit score (p < 0.05), significantly reduced brain infarct volume (p < 0.05), significantly reduced NLRP3 and GSDMD gene expression (p < 0.05), reduced NLRP3, GSDMD, Caspase-1 and other protein expression water, IL-1β, IL-18 inflammatory factor expression were significantly reduced (p < 0.05). Conclusion: Electroacupuncture can improve the symptoms of neurological injury in rats with ischemic stroke model, and may play a neuroprotective role by inhibiting NLRP3/Caspase-1 inflammatory pathway and reducing the expression of cell scorch-related proteins.

Polycystic ovary syndrome (PCOS) is the predominant endocrine disorder among women of re-productive age and represents the leading cause of anovulatory infertility, which imposes a con-siderable health and economic burden. Currently, medications used to treat PCOS can lead to certain adverse reactions, such as affecting fertility and increasing the risk of venous thrombosis. Drug delivery systems utilizing nanomaterials, characterized by prolonged half-life, preci-sion-targeted delivery, enhanced bioavailability, and reduced toxicity, are currently being em-ployed in the management of PCOS. This innovative approach is gaining traction as a favored strategy for augmenting the therapeutic efficacy of medications. Consequently, this paper dis-cusses the roles of nanoparticles, nanocarriers, and targeted ligands within nanomaterial-based drug delivery systems, aiming to identify optimal methodologies for treating PCOS using nano-materials. Additionally, prospective research avenues concerning nanomaterial-based delivery systems in the context of PCOS, as well as the implications of existing insights on the advancement of novel therapies for PCOS, are highlighted.