Current neurovascular research最新文献

{"title":"Headache and Intracranial Aneurysm: A Bidirectional Mendelian Randomization Study.","authors":"Chunlin Ren, Qian Gao, Xinmin Li, Fangjie Yang, Jing Wang, Pengxue Guo, Zhenfei Duan, YuTing Kong, MengYao Bi, Lidian Chen, Yasu Zhang","doi":"10.2174/0115672026380807250530112524","DOIUrl":"https://doi.org/10.2174/0115672026380807250530112524","url":null,"abstract":"<p><strong>Introduction: </strong>Headaches affect up to 95% of individuals during their lifetime and are a major global cause of disability. Intracranial Aneurysm (IA) is a cerebrovascular disorder affecting approximately 3.2% of the general population. Observational studies have suggested an association between headaches and IA, but the causal relationship remains unclear. This Mendelian Randomization (MR) analysis aims to elucidate the causal relationship between headaches and IA.</p><p><strong>Methods: </strong>A two-sample bidirectional Mendelian Randomization (MR) analysis was performed using publicly available Genome-Wide Association Study (GWAS) data to assess the causal relationships between IA and four headache subtypes, namely, Chronic Headache (CH), Tension- Type Headache (TTH), Migraine Without Aura (MO), and Migraine With Aura (MA). The inverse variance weighted method was employed as the primary method, with sensitivity analyses conducted to evaluate the robustness of the results. Mediation analysis was performed to investigate the potential mediating role of hypertension.</p><p><strong>Results: </strong>The MR analysis revealed that MO was associated with an increased risk of aneurysmal Subarachnoid Hemorrhage (aSAH) (Odds Ratio [OR] = 1.422, 95% Confidence Interval [CI]: 1.054-1.918, and P = 0.021), while MA (OR = 1.527, 95% CI: 1.115-2.091, and P = 0.008) was associated with an elevated risk of unruptured IA (uIA). Mediation analysis indicated that hypertension did not significantly mediate these associations.</p><p><strong>Discussion: </strong>This study highlights the potential role of MO in aSAH and MA in uIA, where hypertension does not serve as a significant mediator. Further research is necessary to investigate the underlying mechanisms, which may offer valuable insights into the prevention and management of IA.</p><p><strong>Conclusion: </strong>Bidirectional MR analysis of four headache subtypes and IA provides evidence that MO is associated with an increased risk of aSAH, while MA is linked to a higher risk of uIA. These findings contribute to a better understanding of the complex relationship between headaches and IA.</p>","PeriodicalId":93965,"journal":{"name":"Current neurovascular research","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144228041","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Relationship between Preoperative and Postoperative Peripheral Oxygen Saturation and Malignant Brain Edema in Stroke Patients Undergoing Mechanical Thrombectomy.","authors":"Shuhong Yu, Jinping Yang, Bo Jiang, Zhiliang Guo, Goudong Xiao","doi":"10.2174/0115672026376290250530071306","DOIUrl":"https://doi.org/10.2174/0115672026376290250530071306","url":null,"abstract":"<p><strong>Introduction: </strong>As the fifth vital sign, peripheral oxygen saturation (SpO2) remains understudied in acute ischemic stroke (AIS) patients undergoing mechanical thrombectomy (MT). This study aimed to investigate the association between perioperative SpO2 levels and malignant brain edema (MBE) development in MT-treated AIS patients.</p><p><strong>Methods: </strong>We retrospectively analyzed consecutive stroke patients who achieved successful recanalization through MT between May 2017 and February 2023. Noninvasive SpO2 measurements were obtained pre- and postoperatively. Regression analysis was carried out to assess the association between preoperative, postoperative, and combined SpO2 (stratified into four groups based on SpO2 median values: HL, high preoperative/low postoperative; LL, low/low; HH, high/high; and LH, low/high) and MBE. DeLong's test was conducted to compare the predictive value of combined SpO2 with that of preoperative or postoperative SpO2 alone.</p><p><strong>Results: </strong>Among 376 patients, 84 (22.34%) patients developed MBE. Although preoperative SpO2 was not independently associated with MBE (OR: 0.88; 95% CI: 0.78-1.00; p =0.0583), postoperative SpO2 was independently correlated with MBE (OR: 1.48; 95% CI: 1.01-2.18; p =0.0440). The LH group demonstrated 5.33-fold higher MBE risk versus HL (95% CI: 1.80- 15.82; Ptrend =0.0043). Combined SpO2 assessment outperformed preoperative measurements alone (0.6316 vs. 0.5478, p =0.0382) and trended towards superiority over postoperative values (0.6316 vs. 0.6022, p =0.0541).</p><p><strong>Discussion: </strong>Preoperative and postoperative SpO2 exhibit divergent impacts on MBE, likely reflecting distinct pathophysiology. Preoperative hypoxia may exacerbate ischemic core expansion, while postoperative hyperoxia could augment reperfusion injury via reactive oxygen species. The LH pattern (low pre-/high post-MT SpO2) highlights a high-risk phenotype for MBE.</p><p><strong>Conclusion: </strong>Preoperative and postoperative SpO2 differentially influence MBE development, suggesting distinct pathophysiological mechanisms during thrombectomy phases.</p>","PeriodicalId":93965,"journal":{"name":"Current neurovascular research","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144228042","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Muscone Reduces OGD/R-Induced Hyperpermeability of the Brain Endothelial Barrier by Activating the PKA/RHOA/MLC Pathway.","authors":"Ziteng Yang, Yuanqi Zuo, Guangyun Wang, Ning Wang","doi":"10.2174/0115672026377602250520063326","DOIUrl":"https://doi.org/10.2174/0115672026377602250520063326","url":null,"abstract":"<p><strong>Background: </strong>The endothelial barrier is composed of brain microvascular endothelial cells (BMECs) and tight junction (TJ) proteins. Musk is a valuable ingredient in Traditional Chinese Medicine (TCM). It is used in the treatment of stroke because of its ability to induce resuscitation. The core component of musk is muscone. Previous studies have evidenced that muscone may be involved in the treatment of ischemic stroke (IS), but the underlying mechanism is still unclear. The main objective of this study was to explore the protective effect of muscone on OGD/R-induced endothelial barrier disruption and determine its underlying mechanism.</p><p><strong>Methods: </strong>OGD/R-induced damage to BMECs was assessed using the MTT and LDH assays. The apoptosis level in BMECs was determined using western blot and Hoechst staining. Western blot, immunofluorescence, and phalloidin staining were used to assess the expressions of TJ proteins and pathway proteins expression. A monolayer cell barrier was constructed using BMECs in vitro, and the permeability of the barrier was assessed by TEER as well as the transmissivity of sodium fluorescein. Molecular docking, DARTS, and CETSA were used to verify the regulatory effect of muscone on the pathway.</p><p><strong>Results: </strong>Muscone reduced OGD/R-induced apoptosis of BMEC cells, inhibited the degradation of TJ proteins, promoted the coherent expression of ZO-1 on the membrane, and restored TEER. Mechanistic studies showed that H-89 reversed the promoting effects of muscone on pathway proteins and promoted the disassembly of the actin cytoskeleton, which, in turn, promotes BMEC apoptosis and TJ protein degradation, ultimately disrupting the endothelial barrier.</p><p><strong>Conclusion: </strong>We demonstrated that muscone could reduce OGD/R-induced hyperpermeability of the brain endothelial barrier by activating the PKA/RHOA/MLC pathway.</p>","PeriodicalId":93965,"journal":{"name":"Current neurovascular research","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144201238","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Does Hyperdense Middle Cerebral Artery Sign Predict the Prognosis of Patients Undergoing Emergency Endovascular Treatment?","authors":"Pian Wang, Jin Fan, Weiping Wang, Yangmei Chen","doi":"10.2174/0115672026332288241223114339","DOIUrl":"https://doi.org/10.2174/0115672026332288241223114339","url":null,"abstract":"<p><strong>Background: </strong>Hyperdense Middle Cerebral Artery (HMCAS) is one of the early CT signs of acute Ischemic Stroke (AIS) in patients with large vessel occlusion (LVO). Whether HMCAS is an accurate predictor of functional outcomes in LVO-AIS patients still needs to be further studied. The aim of this study was to analyze the predictive ability of HMCAS on functional outcomes in LVO-AIS patients who underwent emergency endovascular treatment with or without intravenous thrombolysis (IVT).</p><p><strong>Methods: </strong>The clinical and imaging data in LVO-AIS patients who underwent emergency endovascular treatment with or without IVT were retrospectively analyzed. The patients were divided into HMCAS+ group and HMCAS- group according to the presence or absence of HMCAS on initial CT. The endpoint was the 90-day Modified Rankin Scale (mRS) and multivariate logistic ordinal regression was used to determine the association between the presence of HMCAS and 90-day mRS.</p><p><strong>Results: </strong>A total of 173 middle cerebral artery (MCA) LVO-AIS patients were recruited for this study, with 69 (39.88%) in the HMCAS+ group and 104 (60.12%) in the HMCAS- group. The mean age of the participants was 68.98±13.529 years, with 89 (49.71%) being male and 67 (38.73%) receiving intravenous thrombolysis. Multivariate logistic regression of the presence of HMCAS (OR, 1.240 95% CI, 0.693-2.219 P =0.511) was not significantly associated with the 90-- day mRS score.</p><p><strong>Conclusion: </strong>HMCAS may not be a predictor of 90-day mRS in MCA LVO-AIS patients. However HMCAS+ group patients had higher stroke severity before IVT and emergency endovascular treatment. In the era of emergency endovascular treatment the factors affecting the prognosis of LVO-AIS may be different from those of the past.</p>","PeriodicalId":93965,"journal":{"name":"Current neurovascular research","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144082886","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"WITHDRAWN: Primary Changes in Corneal Nerve Fiber Structure in Patients with Primary Glaucoma and Related Influencing Factors","authors":"Mingming Cai, Jie Zhang, Lin Xie","doi":"10.2174/0115672026340315241126041735","DOIUrl":"10.2174/0115672026340315241126041735","url":null,"abstract":"<p><p>The article has been withdrawn at the request of the authors as they could not fulfill the editorial requirements from the editorial office of the journal Current Neurovascular Research.</p><p><p>Bentham Science apologizes to the readers of the journal for any inconvenience this may have caused.</p><p><p>The Bentham Editorial Policy on Article Withdrawal can be found at https://benthamscience.com/editorial-policies-main.php</p><p><strong>Bentham science disclaimer: </strong>It is a condition of publication that manuscripts submitted to this journal have not been published and will not be simultaneously submitted or published elsewhere. Furthermore, any data, illustration, structure or table that has been published elsewhere must be reported, and copyright permission for reproduction must be obtained. Plagiarism is strictly forbidden, and by submitting the article for publication the authors agree that the publishers have the legal right to take appropriate action against the authors, if plagiarism or fabricated information is discovered. By submitting a manuscript the authors agree that the copyright of their article is transferred to the publishers if and when the article is accepted for publication.</p>","PeriodicalId":93965,"journal":{"name":"Current neurovascular research","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142775858","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibition of Circ0001679 Alleviates Ischemia/Reperfusion-induced Brain Injury via miR-216/TLR4 Regulatory Axis.","authors":"Chenrui Zhang, Liaoyu Li, Feng Wang, Hailong Du, Xiaoliang Wang, Xiaoyu Gu, Xinlei Liu, Haie Han, Jianliang Wu, Jianping Sun","doi":"10.2174/0115672026352738241205105129","DOIUrl":"10.2174/0115672026352738241205105129","url":null,"abstract":"<p><strong>Background: </strong>Stroke, primarily known as ischemic stroke, is a leading cause of mortality and disability worldwide. Reperfusion after the ischemia stroke resolves is necessary for maintaining the health of brain tissues; however, it also induces inflammation and oxidative stress, resulting in brain injury. This study aimed to investigate the role of circ0001679 in the pathology of I/R (Ischemia/Reperfusion)-induced brain injury and explore its therapeutic potential for I/R injury.</p><p><strong>Methods: </strong>The Oxygen-Glucose Deprivation/Re-oxygenation (OGD/R) model was employed in primary mouse astrocytes, and the Middle Cerebral Artery Occlusion (MCAO) model was established in mice to mimic ischemia-reperfusion-induced injury. Si-circ0001679, anti-miR- 216, and TLR4 ORF-clone were transfected either in cells or mice to study the molecular mechanisms during I/R-induced injury. Inflammation and oxidative stress were monitored after treatment.</p><p><strong>Results: </strong>Upregulated gene expression of circ0001679 was noticed in both OGD/R-treated primary mouse astrocytes and MCAO-induced mouse brain tissue. Silencing circ0001679 reduced cellular damage, inflammation, and oxidative stress induced by OGD/R treatment. Knocking down of circ0001679 alone with either miR-216 inhibition or TLR4 overexpression increased the inflammation response and oxidative stress compared to circ0001679 silencing only. Moreover, inhibition of circ0001679 attenuated brain injury in MCAO-treated mice via reduced infarction, neuronal damage, apoptosis, inflammation, and oxidative stress.</p><p><strong>Conclusion: </strong>This study unveiled a novel regulatory axis of circ0001679-miR-216-TLR4 in I/Rinduced brain injury. Targeting circ0001679 may represent a promising therapeutic strategy for I/R-induced brain injury.</p>","PeriodicalId":93965,"journal":{"name":"Current neurovascular research","volume":" ","pages":"472-482"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142883993","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Electroacupuncture Serum Protects against Blood-brain Barrier Damage after Ischemic Stroke by Regulating Pericytes <i>in vitro</i>.","authors":"Hanrui Zhang, Hequn Lyv, Yaoting Feng, Yongjun Peng","doi":"10.2174/0115672026361204241115112340","DOIUrl":"10.2174/0115672026361204241115112340","url":null,"abstract":"<p><strong>Background: </strong>Electroacupuncture (EA) exerts a protective role in Blood-brain Barrier (BBB) damage after ischemic stroke, but whether this effect involves the regulation of the pericytes <i>in vitro</i> is unclear.</p><p><strong>Methods: </strong>The <i>in vitro</i> BBB models were established with brain microvascular endothelial cells (BMECs) and pericytes, and the co-cultured cells were randomly divided into three groups: the control group, oxygen-glucose deprivation/reoxygenation (OGD/R) group and EA group. OGD/R was performed to simulate cerebral ischemia-reperfusion <i>in vitro</i>. EA serum was prepared by EA treatment at the \"Renzhong\" (GV26) and \"Baihui\" (GV20) acupoints in middle cerebral artery occlusion/ reperfusion rats. Furthermore, the characteristics of BMECs and pericytes were identified with immunological staining. The cell morphology of the BBB model was observed using an inverted microscope. The function of BBB was measured with transendothelial electrical resistance (TEER) and sodium fluorescein, and the viability, apoptosis, and migration of pericytes were detected by cell counting kit-8, flow cytometry, and Transwell migration assay.</p><p><strong>Results: </strong>BMECs were positive staining for Factor-VIII, and pericytes were positive staining for the α-SMA and NG2. EA serum improved cell morphology of the BBB model, increased TEER and decreased sodium fluorescein in OGD/R condition. Besides, EA serum alleviated pericytes apoptosis rate and migration number, and enhanced pericytes viability rate in OGD/R condition.</p><p><strong>Conclusion: </strong>EA serum protects against BBB damage induced by OGD/R in vitro, and this protection might be achieved by attenuating pericytes apoptosis and migration, as well as enhancing pericytes viability. The findings provided new evidence for EA as a medical therapy for ischemic stroke.</p>","PeriodicalId":93965,"journal":{"name":"Current neurovascular research","volume":" ","pages":"491-502"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142735369","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Microthrombosis at the Ultra-early Stages after Experimental Subarachnoid Hemorrhage Results in Early Brain Injury.","authors":"Masaki Kumagai, Yusuke Egashira, Nozomi Sasaki, Shinsuke Nakamura, Yoshiki Kuse, Hirohumi Matsubara, Yukiko Enomoto, Tsuyoshi Izumo, Hideaki Hara, Masamitsu Shimazawa","doi":"10.2174/0115672026362878241220065541","DOIUrl":"10.2174/0115672026362878241220065541","url":null,"abstract":"<p><strong>Introduction: </strong>Early Brain Injury (EBI) significantly contributes to poor neurological outcomes and death following subarachnoid hemorrhage (SAH). The mechanisms underlying EBI post-SAH remain unclear. This study explores the relationship between serial cerebral blood flow (CBF) changes and neurological symptoms, as well as the mechanisms driving CBF changes in the ultra-early stages after experimental SAH in mice.</p><p><strong>Methods: </strong>SAH was induced by endovascular perforation in male ddY mice. Mice were sacrificed at 6, 12, 24, and 48 h after behavioral tests using the modified neurological score and grid walking test, and CBF was measured via Laser Speckle Flow Imaging (LSFI). Neurofunctional evaluation, CBF analysis, and Western blotting were used to assess SAH-induced damage.</p><p><strong>Results: </strong>Neurological symptoms were significantly worse at 12 h post-SAH compared to sham (9.5 ± 1.7 vs. 25.6 ± 0.63, respectively; p < 0.0001). CBF was significantly reduced at 12 h post- SAH compared to sham (35.34 ± 8.611 vs. 91.06 ± 12.45, respectively; p < 0.0001). Western blotting revealed significantly elevated thrombin and matrix metalloproteinase 9 levels 12 h post-SAH (p < 0.05).</p><p><strong>Conclusion: </strong>Our results suggest that microthrombus formation peaked at 12 h post-SAH, potentially causing EBI and worsening neurological symptoms. Microthrombus formation in the ultraearly stages may represent a novel therapeutic target for managing EBI.</p>","PeriodicalId":93965,"journal":{"name":"Current neurovascular research","volume":" ","pages":"529-536"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142934099","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Etiologies and Risk Factors by Sex and Age in Young Adult Patients with Ischemic Stroke.","authors":"Linrui Huang, Yanhua Wang, Yanan Wang, Simiao Wu","doi":"10.2174/0115672026370844241223080012","DOIUrl":"10.2174/0115672026370844241223080012","url":null,"abstract":"<p><strong>Aim: </strong>The aim of this study was to explore etiologies and risk factors by age and sex in young adult patients with ischemic stroke.</p><p><strong>Methods: </strong>We recruited patients with ischemic stroke aged between 18 and 49 years. We assessed pathological etiologies by the Trial of Org 10,172 in Acute Stroke Treatment (TOAST) classification and risk factors by the International Pediatric Stroke Study (IPSS) classification. We explored the distribution of etiologies and risk factors by age and sex and investigated baseline features associated with functional outcomes at 3 months.</p><p><strong>Results: </strong>Of 8521 stroke patients consecutively admitted, 1017 patients (11.9%) aged between 18-49 years, of whom large artery atherosclerosis was the most common etiology (n=375, 36.9%), followed by other determined cause (n=194, 19.1%) and undetermined cause (n=184, 18.1%). Compared to male patients, female patients had more cardioembolism (16.34% vs 8.42%) and less small artery occlusion (8.56% vs 17.76%). As age increased, the proportions of large artery atherosclerosis (P <0.001) and small artery occlusion (P <0.001) increased, and the proportion of other determined causes decreased (P <0.001). Of 184 patients with undetermined causes, 173 (94.0%) had at least one IPSS risk factor. A higher serum level of D-dimer at baseline was associated with an increased risk of unfavorable outcome (OR 1.118, 95% CI 1.052- 1.189), adjusting for the effect of age and stroke severity.</p><p><strong>Conclusion: </strong>Approximately one-fifth of young patients with ischemic stroke had undetermined etiology, for whom the IPSS classification helps to explore risk factors. A higher level of Ddimer was associated with a higher risk of unfavorable outcomes at 3 months.</p>","PeriodicalId":93965,"journal":{"name":"Current neurovascular research","volume":" ","pages":"574-583"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142933900","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Basic Fibroblast Growth Factor-releasing Polyglycolic Acid Duras Improve Neurological Function after Cerebral Infarction.","authors":"Yoshiro Ito, Ayako Oyane, Hideo Tsurushima, Yuji Matsumaru, Eiichi Ishikawa","doi":"10.2174/0115672026371969241224112004","DOIUrl":"10.2174/0115672026371969241224112004","url":null,"abstract":"<p><strong>Objective: </strong>Regenerative therapy using stem cells to treat cerebral infarction is currently in the research phase. However, this method is costly. It also faces other significant challenges, including optimization of timing, delivery methods, and dosage. Therefore, more practical and effective therapies are required. Bioabsorbable artificial dura mater made from nonwoven Polyglycolic Acid (PGA) fabric is used clinically to treat cerebral infarction. Basic Fibroblast Growth Factor (bFGF) has attracted considerable attention as a potential therapeutic candidate for the treatment of cerebral infarctions. In this study, we aimed to prepare a bFGF-releasing PGA dura mater and investigate its therapeutic efficacy for the recovery of neurological function in a mouse model of focal cerebral infarction.</p><p><strong>Methods: </strong>An artificial dura mater (Durawave) made from nonwoven PGA fabric was subjected to oxygen plasma treatment, followed by bFGF adsorption. The release of bFGF from the resulting PGA dura mater was evaluated <i>in vitro</i> using enzyme-linked immunosorbent assays. bFGF-releasing PGA dura mater was placed at the site of induced cerebral infarctions in mice. Neurological function was assessed 14 days after insertion, followed by a histological assessment.</p><p><strong>Results: </strong>The prepared PGA dura mater released bFGF in a dose-dependent manner. Neurological function in the bFGF-treated groups was significantly better than that in the control group. bFGFreleasing PGA dura mater also significantly increased the number of neural progenitor cells in the peri-infarct cortex and striatum and showed a trend toward promoting angiogenesis.</p><p><strong>Conclusion: </strong>bFGF-releasing PGA dura mater improved neurological function in a mouse model of focal cerebral infarction.</p>","PeriodicalId":93965,"journal":{"name":"Current neurovascular research","volume":" ","pages":"584-594"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143026214","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}