International Journal of Neuroscience最新文献

{"title":"Bioinformatic identification and clinical validation of VIM and OSM as prognostic biomarkers in cerebral infarction: implications for risk stratification.","authors":"Changyan Fan, Chaosheng Li, Chenyan Sui, Likun Han, Yong Liu","doi":"10.1080/00207454.2025.2601618","DOIUrl":"10.1080/00207454.2025.2601618","url":null,"abstract":"<p><strong>Background: </strong>Reliable molecular biomarkers for predicting cerebral infarction outcomes remain limited, highlighting the need for integrative approaches that bridge bioinformatic discovery with clinical validation.</p><p><strong>Objective: </strong>To identify key differentially expressed genes (DEGs) prognostic for cerebral infarction and evaluate their clinical utility for risk stratification through integrated bioinformatic analysis and prospective cohort validation.</p><p><strong>Methods: </strong>Functional annotation employed GO enrichment and protein-protein interaction network analysis. A prospective cohort enrolled 151 cerebral infarction patients, with peripheral blood samples subjected to qPCR analysis of candidate genes. Prognostic predictive capacity was assessed <i>via</i> multivariable Cox regression, Kaplan-Meier survival analysis, and ROC curve analysis with clinical follow-up data.</p><p><strong>Results: </strong>Five candidate DEGs (VIM, OSM, PTGS2, SOD2, SAMSN1) were identified, enriched in inflammatory response, nitric oxide metabolism, and lipopolysaccharide response pathways. qPCR confirmed significantly elevated VIM, OSM, and PTGS2 expression in poor prognosis group (<i>p</i> < 0.01). Multivariable Cox regression identified VIM (HR = 4.475), OSM (HR = 2.800), and homocysteine (Hcy; HR = 1.120) as independent prognostic risk factors. Kaplan-Meier analysis demonstrated significantly reduced survival in high-expression groups (all <i>p</i> < 0.01). The combined model integrating VIM, OSM, and Hcy achieved superior predictive performance (AUC = 0.811; sensitivity 72.55%, specificity 78.00%, Youden's index 0.506) compared to VIM alone (AUC = 0.760).</p><p><strong>Conclusion: </strong>VIM and OSM exhibit robust bioinformatic associations and stable expression with independent prognostic value in clinical cohorts.</p>","PeriodicalId":14161,"journal":{"name":"International Journal of Neuroscience","volume":" ","pages":"577-590"},"PeriodicalIF":1.5,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145714194","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Beyond the impact: emerging therapies shaping the future of post-concussion recovery.","authors":"Muhammad Liaquat Raza, Syed Tawassul Hassan, Wajiha Fatima, Noorulain Hyder, Zoha Turabee","doi":"10.1080/00207454.2025.2610611","DOIUrl":"10.1080/00207454.2025.2610611","url":null,"abstract":"<p><p>Persistent post-concussion symptoms can greatly affect a person's life, thinking abilities, and their capacity to go back to normal daily tasks. This narrative review gives a detailed look at new treatments for ongoing symptoms after a concussion. It includes methods like brain stimulation, medications, and holistic approaches. We searched for information using PubMed, Embase, and Google Scholar, looking for keywords like 'post-concussion syndrome', 'neuromodulation', 'rehabilitation', 'cognitive behavioral therapy', 'vestibular therapy', and 'medications. 'This review talks about how each therapy works, the proof from clinical trials, and practical tips for using them. Methods like transcranial magnetic stimulation and transcranial direct current stimulation could help improve thinking skills and mood problems. Medicines like amantadine and zolpidem may help treat certain symptoms. Methods like aerobic exercise, balance training, and talk therapy provide overall benefits. The review also points out future areas to explore, like stem cell treatment, using virtual reality for rehab, timing treatments better, and using light therapy. This review looks at new information and trends to help doctors and researchers understand the latest ways to treat ongoing symptoms after a concussion. It also aims to guide future studies in this important field.</p>","PeriodicalId":14161,"journal":{"name":"International Journal of Neuroscience","volume":" ","pages":"600-617"},"PeriodicalIF":1.5,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145849858","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A patent review on traumatic brain injuries (2020-2025).","authors":"Khyati Sharma, Deepak Agrawal, Reema Gabrani","doi":"10.1080/00207454.2026.2620698","DOIUrl":"10.1080/00207454.2026.2620698","url":null,"abstract":"<p><strong>Introduction: </strong>Traumatic brain injury (TBI) remains a leading cause of disability and death worldwide, with no FDA-approved therapies capable of halting or reversing secondary injury cascades.</p><p><strong>Areas covered: </strong>Recent years (2020-2025) have witnessed a surge in patent activity targeting diagnostic innovations, biomarker integration, and therapeutic strategies in TBI. Diagnostic advances include multimodal platforms that combine blood-based biomarkers, imaging modalities, and physiological monitoring to enhance early detection and stratification. Biomarker-driven patents, particularly those centered on glial fibrillary acidic protein (GFAP), ubiquitin C-terminal hydrolase L1 (UCH-L1), neurofilament light chain (NfL), and p-tau, have demonstrated translational value by enabling point-of-care testing and guiding therapeutic decisions. Therapeutic patents encompass a wide range of innovations, including anti-inflammatory and antioxidant agents, metabolic and vascular stabilizers, regenerative approaches, and advanced drug delivery systems designed to bypass the blood-brain barrier. Importantly, multimodal therapeutic strategies that integrate neuroprotection, neuro-restoration, and functional recovery are gaining momentum.</p><p><strong>Expert opinion: </strong>Innovations in patents, such as breath-based sensors, eye-tracking systems, and non-invasive technologies, are expanding the possibilities for rapid, point-of-care testing. On the therapeutic side, patents focusing on monoclonal antibodies, neuroactive steroids, neuroprotective peptides, and site-specific delivery systems show promise; however, most candidates are still in preclinical or early clinical stages.</p>","PeriodicalId":14161,"journal":{"name":"International Journal of Neuroscience","volume":" ","pages":"650-664"},"PeriodicalIF":1.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146029451","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"FAS rs2234767 polymorphism confers protection against glioma: a case-control study in Chinese population.","authors":"Xiuli Huang, Jiang Ran, Li Liang, Weibin Li, Juan Tang, Leping Ning","doi":"10.1080/00207454.2026.2620705","DOIUrl":"10.1080/00207454.2026.2620705","url":null,"abstract":"<p><strong>Background: </strong>Genetic polymorphisms in apoptosis-related genes FAS/FASL may influence susceptibility to glioma, but evidence remains limited, particularly in Chinese populations. This study aimed to investigate the potential association between gene polymorphisms in FAS (rs2234767 and rs1800682) and FASL (rs763110 and rs6700734) and glioma risk in a Chinese cohort.</p><p><strong>Methods: </strong>This case-control study included 107 glioma patients and 110 healthy controls. Four polymorphisms were genotyped using TaqMan real-time PCR. The associations between these genetic variants and glioma risk were evaluated <i>via</i> logistic regression after adjusting for relevant covariates. Furthermore, subgroup analyses stratified by ethnicity, isocitrate dehydrogenase 1 (IDH1) R132H status and histological grade were performed, along with a haplotype-based analysis.</p><p><strong>Results: </strong>The FAS rs2234767 GA genotype was associated with a significantly reduced glioma risk compared to the GG genotype (adjusted OR = 0.461, 95% CI: 0.232-0.917, <i>p</i> = 0.027). This protective effect was particularly evident in the Han subgroup (adjusted OR = 0.275, 95% CI: 0.106-0.716, <i>p</i> = 0.008), IDH1 R132H-positive cases (adjusted OR = 0.362, 95% CI: 0.148-0.884, <i>p</i> = 0.026) and low-grade gliomas (adjusted OR = 0.350, 95% CI: 0.133-0.922, <i>p</i> = 0.034). No notable associations were observed for FASL variants. Haplotype analyses revealed no significant associations.</p><p><strong>Conclusions: </strong>This study suggests a potential protective role of the FAS rs2234767 GA genotype against glioma in the Chinese population, particularly among Han individuals, IDH1 R132H-positive cases and low-grade gliomas. The findings, while insightful, require validation in larger cohorts. Future research should integrate molecular profiling and functional assays to clarify the underlying mechanisms.</p>","PeriodicalId":14161,"journal":{"name":"International Journal of Neuroscience","volume":" ","pages":"686-694"},"PeriodicalIF":1.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146018456","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association between high-density lipoprotein cholesterol to apolipoprotein A-1 ratio and the outcome of ischemic stroke: a retrospective study.","authors":"Linyan Li, Huiming Deng, Zhiyao Xu, Yan Liu, Xianwen Zhang, Qiang Zhou, Bing Xiao, Hua Liu","doi":"10.1080/00207454.2026.2614748","DOIUrl":"10.1080/00207454.2026.2614748","url":null,"abstract":"<p><strong>Background: </strong>High-density lipoprotein cholesterol (HDL-C)/apolipoprotein A-1 (APOA-1) ratio has been identified as a risk factor for cardiovascular disease, cancer, and all-cause mortality. However, data related to ischemic stroke (IS) are lacking. We investigated whether the HDL-C/APOA-1 ratio was associated with 3-month functional outcome in patients with IS.</p><p><strong>Methods: </strong>A retrospective analysis was performed on 674 patients with IS. The 3-month functional outcome was classified as good or poor based on the modified Rankin Scale score (mRS). Logistic regression models (unadjusted and stepwise) were performed to evaluate the correlation between HDL-C/APOA-1 ratio and outcome. Restricted cubic splines evaluated nonlinear relationships, while subgroup analyses explored effect modifications. We assessed the added predictive value of the HDL-C/APOA-1 ratio by comparing nested models using the AUC, NRI, and IDI.</p><p><strong>Results: </strong>The HDL-C/APOA-1 level in the group with poor functional outcomes was higher than that in the group with good functional outcomes (0.99 ± 0.14 vs. 0.94 ± 0.10, <i>p</i> < 0.001). In the multivariable analysis, a higher HDL-C/APOA-1 ratio was identified as an independent factor associated with poor outcome at 3 months (OR 1.50, 95% CI:1.17-1.96, <i>p</i> = 0.003). The odds of poor outcome in the higher HDL-C/APOA-1 quartile increased by 2.44-fold (95% CI:1.30-4.64, <i>p</i> = 0.006) after adjusting for potential confounders compared to lower HDL-C/APOA-1 quartiles. In addition, multivariate-adjusted restricted cubic splines show a positive approach linear pattern of this association.</p><p><strong>Conclusion: </strong>Elevated HDL-C/APOA-1 is independently associated with an increased risk of poor functional outcomes at 3-month in patients with IS.</p>","PeriodicalId":14161,"journal":{"name":"International Journal of Neuroscience","volume":" ","pages":"642-649"},"PeriodicalIF":1.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145933329","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evolving trends and disparities in malnutrition-linked stroke mortality in the United States: insights from CDC WONDER data.","authors":"F N U Sahil, Sahil Jairamani, Muhammad Rafay Shahzad Cheema, Fnu Urooba, Muhammad Ibrahim, Iman Osman Abufatima, Ali Nawaz, Maha Sajjad, Dheeraj Kumar","doi":"10.1080/00207454.2025.2612560","DOIUrl":"10.1080/00207454.2025.2612560","url":null,"abstract":"<p><strong>Background: </strong>Stroke and malnutrition remain significant contributors to preventable mortality in the United States. Stroke is a leading cause of death and disability, while malnutrition, often underrecognized, exacerbates neurological and systemic vulnerability. Characterizing long-term national and subgroup-specific mortality patterns is critical for guiding public health interventions.</p><p><strong>Methods: </strong>Mortality data for stroke and malnutrition were analyzed from 1999 to 2023 using the CDC WONDER database. Age-adjusted mortality rates (AAMR) per 1,000,000 population were calculated and stratified by sex, race/ethnicity, census region, state and urbanization status. Joinpoint regression estimated average annual percent change (AAPC) with 95% confidence intervals (CIs).</p><p><strong>Results: </strong>From 1999 to 2023, 44,368 deaths were attributed to malnutrition and stroke. The overall AAMR rose from 12.11 in 1999 to 14.75 in 2023, with an overall AAPC of 0.88% (95% CI: -0.14 to 1.91). Males had higher AAMRs than females. By race, Non Hispanic (NH) Black experienced the greatest AAMRs, whereas NH Asian had the lowest rates. Regionally, the South showed the highest rate, whereas Northeast had the lowest. Nonmetropolitan areas exceeded metropolitan areas. At the state level, the highest rates were observed in South Dakota and Arkansas, while Massachusetts recorded the lowest rates.</p><p><strong>Conclusion: </strong>From 1999 to 2023, combined mortality from stroke and malnutrition increased modestly nationwide, with enduring disparities across demographics and geography. The highest burdens fell on NH Black individuals, people living in the South and nonmetropolitan areas, and certain central states. These findings highlight the need for region-specific prevention and better access to nutritional and neurological care.</p>","PeriodicalId":14161,"journal":{"name":"International Journal of Neuroscience","volume":" ","pages":"629-641"},"PeriodicalIF":1.5,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145899992","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of intracranial atherosclerotic plaque features with total cerebral small vessel disease burden: a retrospective study in branch atheromatous disease.","authors":"Guisong Zhang, Weigang Luo, Yujuan Dong, Jinyang Wang, Wei Bu, Danlin Meng, Linghui Meng, Huiling Ren","doi":"10.1080/00207454.2025.2597798","DOIUrl":"10.1080/00207454.2025.2597798","url":null,"abstract":"<p><strong>Objective: </strong>We investigated the association between middle cerebral artery atherosclerotic plaque features and cerebral small vessel disease (CSVD) imaging markers as well as the total CSVD burden, in patients with branch atheromatous disease (BAD).</p><p><strong>Methods: </strong>Plaque parameters were quantified using high-resolution magnetic resonance imaging (HR-MRI) with ImageJ software, to characterize distribution, lumen stenosis, remodeling patterns, and other relevant features. Conventional MRI assessed CSVD imaging markers and total CSVD burden. Multivariate logistic regression analysis was performed following adjustment for potential confounders. Receiver operating characteristic (ROC) curve analysis with the DeLong test assessed the predictive value of plaque features for total CSVD burden.</p><p><strong>Results: </strong>Compared with the non-plaque group, the plaque group showed significantly higher proportions of severe white matter hyperintensities (WMHs), cerebral microbleeds (CMBs), and moderate-to-severe CSVD burden (<i>p</i> < 0.05). In multivariate analysis, the presence of plaque was an independent risk factor for WMHs (OR = 2.920), CMBs (OR = 1.995), and moderate-to-severe CSVD burden (OR = 2.853); plaque distribution was an independent risk factor for WMHs (OR = 3.367); eccentric plaques were independent risk factors for lacunar infarction (OR = 8.670) and CMBs (OR = 7.891); positive remodeling (OR = 9.285) and eccentric plaques (OR = 10.355) were independent risk factors for moderate-to-severe CSVD burden. ROC analysis demonstrated plaque vulnerability effectively predicted moderate-to-severe CSVD burden (AUC = 0.8808, <i>p</i> < 0.05).</p><p><strong>Conclusion: </strong>In ischemic stroke patients, distinct intracranial atherosclerotic stenosis (ICAS) plaque features correlate with specific CSVD phenotypes. Vulnerable plaques not only significantly increase total CSVD burden but also effectively predict CSVD severity. These findings elucidate how ICAS influences CSVD burden progression from an HR-MRI perspective and facilitate clinical risk stratification.</p>","PeriodicalId":14161,"journal":{"name":"International Journal of Neuroscience","volume":" ","pages":"565-576"},"PeriodicalIF":1.5,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145677449","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lactate dehydrogenase-to-albumin ratio predicts ischemic stroke recurrence in patients with symptomatic carotid artery stenosis: a pilot retrospective cohort study.","authors":"Feng Ye, Nana Ren, Haitao Fang, Ke Shen","doi":"10.1080/00207454.2025.2605267","DOIUrl":"10.1080/00207454.2025.2605267","url":null,"abstract":"<p><strong>Aim: </strong>Symptomatic carotid artery stenosis (SCAS) patients face a high risk of ischemic stroke (IS) recurrence. This study evaluates the prognostic value of the serum lactate dehydrogenase (LDH)-to-albumin ratio (L/A) for predicting IS recurrence among SCAS patients.</p><p><strong>Methods: </strong>In this retrospective study (January 2020-January 2023), 307 conservatively managed SCAS patients were stratified into non-recurrence (<i>n</i> = 238) and recurrence (<i>n</i> = 69) groups based on 24-month follow-up. Serum LDH and albumin were measured, and L/A was calculated. Relationships between L/A and plaque neovascularization-related parameters (peak intensity, AUCTC, CAS rate) were assessed using Pearson correlation. Independent risk factors were determined with multivariate Cox regression, while the predictive performance and risk stratification of L/A were evaluated with ROC and Kaplan-Meier curves.</p><p><strong>Results: </strong>Significant differences existed in age, hypertension, hyperlipidemia, systolic blood pressure, low-density lipoprotein cholesterol, albumin, peak intensity, AUCTC, CAS rate, vulnerable plaques, and medication adherence between the two groups. Recurrent patients exhibited higher L/A (<i>p</i> < 0.005). L/A correlated positively to peak intensity (<i>r</i> = 0.323), AUCTC (<i>r</i> = 0.450), and CAS rate (<i>r</i> = 0.529; all <i>p</i> < 0.001). Hyperlipidemia, vulnerable plaques, peak intensity, CAS rate, and elevated L/A were independent risk factors for IS recurrence in SCAS patients. L/A could assist in predicting IS recurrence in SCAS patients (AUC: 0.801; sensitivity: 63.77%; specificity: 85.71%). High L/A significantly increased 2-year recurrence risk in SCAS patients.</p><p><strong>Conclusion: </strong>Elevated L/A potentially aids in predicting IS recurrence in SCAS patients and correlates to plaque neovascularization.</p>","PeriodicalId":14161,"journal":{"name":"International Journal of Neuroscience","volume":" ","pages":"591-599"},"PeriodicalIF":1.5,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145768054","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Graph-theoretical analysis of resting-state EEG networks differentiates Alzheimer's disease and frontotemporal dementia.","authors":"Li Zhu, Yue Pan, Zi-Liang Wang","doi":"10.1080/00207454.2026.2620704","DOIUrl":"10.1080/00207454.2026.2620704","url":null,"abstract":"<p><strong>Background: </strong>Alzheimer's disease (AD) and frontotemporal dementia (FTD) are neurodegenerative diseases with overlapping symptoms, complicating diagnosis. EEG-derived brain connectivity metrics, based on network neuroscience, can quantify brain network organization, but comparisons between AD and FTD using standardized EEG datasets are limited.</p><p><strong>Methods: </strong>We analyzed a publicly available EEG dataset consisting of 36 AD patients, 23 FTD patients, and 29 healthy controls (HCs). Resting-state eyes-closed and eyes-open EEGs were analyzed across delta, theta, alpha, and beta bands. Phase-locking values (PLV) estimated functional connectivity between 19 electrodes, and graph-theory metrics were derived using the Brain Connectivity Toolbox. Group differences were assessed using ANOVAs with FDR correction, followed by Tukey tests.</p><p><strong>Results: </strong>AD patients showed reduced global efficiency and small-worldness, especially in the alpha and beta bands under eyes-closed conditions, indicating decreased integration. FTD patients exhibited localized network disruptions in frontal and central regions, particularly reduced node degree and local efficiency at F3/F4 and Pz electrodes, suggesting region-specific dysfunction. These differences were more prominent in the eyes-closed state.</p><p><strong>Conclusion: </strong>EEG graph-theory analysis revealed distinct network alterations in AD and FTD. AD showed impaired global integration and loss of small-world architecture, while FTD demonstrated region-specific disruptions. These findings suggest that EEG graph metrics may serve as cost-effective biomarkers for differentiating dementia subtypes and understanding disease-specific network dysfunction.</p>","PeriodicalId":14161,"journal":{"name":"International Journal of Neuroscience","volume":" ","pages":"677-685"},"PeriodicalIF":1.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146029481","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Liproxstatin-1 ameliorates cerebral ischemia-reperfusion injury through inhibiting ferroptosis.","authors":"Lie Xiong, Yuting Jin, Jingruo Zhang, Hanqiang Shi, Gaofeng Zhu, Ping Zhu, Yanlin Liu, Kaitao Luo","doi":"10.1080/00207454.2026.2620703","DOIUrl":"10.1080/00207454.2026.2620703","url":null,"abstract":"<p><strong>Objective: </strong>This study intends to investigate the protective impact of liproxstatin-1 against cerebral ischemia-reperfusion injury (CIRI) in rats and the corresponding underlying mechanism.</p><p><strong>Methods: </strong>CIRI rat models were constructed. Pathological changes in tissues were assessed at multiple levels, including infarct area, neuronal activity, and iron content through 2,3,5-triphenyl tetrazolium chloride (TTC) staining, Nissl staining and Prussian blue (PB) staining. The expression of oxidative damage factors and key ferroptosis-related genes was assessed by enzyme-linked immunosorbent assay (ELISA), quantitative real-time PCR (qPCR) or western blot (WB). Rat brain tissues were subjected to bulk RNA sequencing (bulk RNA-seq) analysis. Finally, <i>in vitro</i> oxygen-glucose deprivation/reoxygenation (OGD/R) models were established, and the inhibitory effect of liproxstatin-1 on ferroptosis was identified by measuring cell viability, Fe²⁺ levels and lipid peroxidation.</p><p><strong>Results: </strong><i>In vivo</i> experiments demonstrated that liproxstatin-1 markedly improved neurological function and neuronal pathological damage in CIRI rats, while reducing iron content and oxidative damage. Bulk RNA-seq analysis revealed that differentially expressed genes (DEGs) were mainly enriched in the IL-17 signaling pathway, ether lipid metabolism, TNF signaling pathway and ferroptosis. Consistently, qPCR and WB results showed that liproxstatin-1 treatment increased the expression of FTH1 and GPX4, while decreasing the expression of NOX1, ACSL4, COX2 and TFR1 in rat brain tissues. <i>In vitro</i> experiments further demonstrated that liproxstatin-1 significantly enhanced cell viability and reduced Fe²⁺ and reactive oxygen species (ROS) levels.</p><p><strong>Conclusions: </strong>Liproxstatin-1 inhibits the process of ferroptosis and alleviates CIRI in rats.</p>","PeriodicalId":14161,"journal":{"name":"International Journal of Neuroscience","volume":" ","pages":"665-676"},"PeriodicalIF":1.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146097109","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}