{"title":"L-3n-butylphthalide maintains BBB permeability and attenuates cerebral ischemia-reperfusion injury in rats by increasing PGC-1<i>α</i> levels.","authors":"Yu Wang, Xiangsong Shi, Liling Wu, Hongfu Tian","doi":"10.1080/00207454.2025.2545534","DOIUrl":"10.1080/00207454.2025.2545534","url":null,"abstract":"<p><strong>Aim: </strong>The aim of the present study was to investigate the possible mechanisms of DL-3-n-butylphthalide (NBP) in maintaining the stability of the blood-brain barrier (BBB) and attenuating cerebral ischemia-reperfusion injury (CIRI) by increasing the levels of PGC-1<i>α</i>.</p><p><strong>Methods: </strong>A model of middle cerebral artery occlusion/reperfusion (MCAO/R) injury was established using Sprague-Dawley rats. The rats were divided into sham, MCAO/R, NBP, Vehicle and SR-18292 groups. 2,3,5-Triphenyltetrazolium chloride staining, hematoxylin and eosin (H&E) staining, and Evans Blue staining were performed to observe the volume of cerebral infarction, status of pathological injury, and BBB permeability of the brain tissue, respectively. Immunofluorescence staining and western blot analysis were performed to evaluate the expression of vascular endothelial cell markers (vWF and CD31), tight junction (TJ) protein markers (claudin5 and occludin), and PGC-1<i>α</i>.</p><p><strong>Results: </strong>H&E staining showed that the brain tissues of MCAO/R rats showed worsening vacuolar degeneration and necrosis. NBP reduced infarct volume, decreased the level of BBB extravasation, increased vascular density, and promoted the expression of TJs. Concurrently, NBP activated PGC-1<i>α</i> levels in rats subjected to MCAO/R. Downregulation of PGC-1<i>α</i> levels by PGC-1<i>α</i> inhibitors (SR-18292) could promote BBB permeability, infarct volume, and neurological deficits in the MCAO/R model.</p><p><strong>Conclusions: </strong>The present study demonstrates that NBP plays a role in maintaining the stability of the BBB and attenuates CIRI by increasing PGC-1<i>α</i> levels as well as by increasing the levels of vascular endothelial cells and TJ markers.</p>","PeriodicalId":14161,"journal":{"name":"International Journal of Neuroscience","volume":" ","pages":"1-12"},"PeriodicalIF":1.5,"publicationDate":"2025-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144812054","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":"Analysis of the clinical effects of the transvertebral anterior approach for contralateral C7 nerve translocation in treating Central upper limb paralysis: a retrospective study.","authors":"Shichang Guo, Bo Zhang, Xiaohui Liu, Jiabo Xiao, Binhong Li, Wandong Ma, Jinsheng Kang, Changzheng Dong","doi":"10.1080/00207454.2025.2544803","DOIUrl":"10.1080/00207454.2025.2544803","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the clinical efficacy of the transvertebral anterior approach to contralateral C7 nerve translocation for treating patients with upper limb spastic hemiparesis caused by central nerve injury.</p><p><strong>Methods: </strong>Clinical data from 30 patients with central upper limb spastic hemiplegia were included in the study. All patients underwent rehabilitation exercises before surgery. As no significant improvement in motor function or muscle tone of the paralyzed upper limb was observed, contralateral C7 nerve translocation was performed. Changes in motor function of the paralyzed upper limb were assessed using the Fugl-Meyer Motor Function Assessment Scale (FMA) and Brunnstrom Staging Scale (BSS). Changes in muscle tone were evaluated using the Modified Ashworth Spasticity Rating Scale (MAS). Generalized estimating equation (GEE) analysis was performed using the preoperative FMA, BSS, and MAS scores as baseline values to assess improvements in motor function and muscle tone at 6 and 12 months postoperatively.</p><p><strong>Results: </strong>Significant differences were observed in motor function (FMA score and BSS stage) and muscle tone (MAS score) of the paralyzed upper limb at 6 and 12 months post-surgery compared to baseline (<i>p</i> < 0.05) in 30 patients. Recovery of the paralyzed upper limb showed a time-dependent cumulative effect, with greater improvement observed at 12 months post-surgery than at 6 months. Recovery of limb function exhibited progressive improvement from the proximal to the distal end.</p><p><strong>Conclusion: </strong>Contralateral C7 nerve translocation helps improve central upper limb spastic paralysis and reduce muscle spasticity, thereby enhancing upper limb motor function.</p>","PeriodicalId":14161,"journal":{"name":"International Journal of Neuroscience","volume":" ","pages":"1-9"},"PeriodicalIF":1.5,"publicationDate":"2025-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144821422","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}
Shahad Mohammed Dhiaa Younis, Abdulkareem Shareef, Ashok Kumar Bishoyi, R Roopashree, Aditya Kashyap, Atreyi Pramanik, Subhashree Ray, Zilola Mavlyanova, Hayder Naji Sameer, Ahmed Yaseen, Zainab H Athab, Mohaned Adil
{"title":"Serum tyrosine associates with increased CSF Aβ42, reduced Aβ deposition, and cognitive improvement in MCI: modulation by confounding factors.","authors":"Shahad Mohammed Dhiaa Younis, Abdulkareem Shareef, Ashok Kumar Bishoyi, R Roopashree, Aditya Kashyap, Atreyi Pramanik, Subhashree Ray, Zilola Mavlyanova, Hayder Naji Sameer, Ahmed Yaseen, Zainab H Athab, Mohaned Adil","doi":"10.1080/00207454.2025.2544791","DOIUrl":"10.1080/00207454.2025.2544791","url":null,"abstract":"<p><p>Tyrosine, a precursor to dopamine, norepinephrine, and epinephrine, has shown mixed results in cognitive impairment studies, suggesting a complex role in mild cognitive impairment (MCI). This study is the first to explore its relationship with CSF amyloid-beta (Aβ) 42, Aβ accumulation, and cognitive function in MCI (<i>n</i> = 251).</p><p><p>Cognitive function was assessed using ADAS-Cog, serum tyrosine by UPLC-MS/MS, Aβ42 by ELISA, and Aβ accumulation <i>via</i> florbetapir PET with SUVr, all validated with quality control. Two analysis models were used: Model 1 (unadjusted) and Model 2 (adjusted for age, gender, education, handedness, and ApoE status).</p><p><p>The study found a significant positive link between serum tyrosine levels and CSF Aβ42, with higher tyrosine levels associated with increased Aβ42, independent of demographic and genetic factors. Mediation analysis revealed that in Model 1, higher serum tyrosine was associated with improved cognitive function, potentially through increased CSF Aβ42 levels. However, this association was not present after adjusting for confounders in Model 2. Further investigation of Aβ accumulation in specific brain regions (global, frontal, temporal, and parietal lobes) found that, in Model 1, higher serum tyrosine was linked to reduced Aβ accumulation in the frontal and temporal lobes, wich in turn correlated with better cognitive function. Yet, after adjusting for confounders in Model 2, these effects were no longer significant.</p><p><p>Overall, the findings suggest that while serum tyrosine may influence cognitive improvement in MCI through its relationship with CSF Aβ42 and Aβ accumulation, these effects are strongly influenced by demographic and genetic factors.</p>","PeriodicalId":14161,"journal":{"name":"International Journal of Neuroscience","volume":" ","pages":"1-16"},"PeriodicalIF":1.5,"publicationDate":"2025-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144789075","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}
Yao Lu, Yang Li, Wenhao Su, Yan Lv, Zhouhong Zheng, Ameng Zhao, Zhongqing Wang
{"title":"Vagus nerve stimulation ameliorates learning-memory deficits and suppresses neuronal apoptosis via the ERK/CREB/BDNF signaling pathway in epileptic rats.","authors":"Yao Lu, Yang Li, Wenhao Su, Yan Lv, Zhouhong Zheng, Ameng Zhao, Zhongqing Wang","doi":"10.1080/00207454.2025.2542882","DOIUrl":"10.1080/00207454.2025.2542882","url":null,"abstract":"<p><strong>Purpose: </strong>This study aimed to evaluate the impact of vagus nerve stimulation (VNS) on learning, memory and neuronal apoptosis in epileptic rats, and to investigate the involvement of the ERK/CREB/BDNF signaling pathway.</p><p><strong>Methods: </strong>Epilepsy was induced in rats <i>via</i> lithium chloride-pilocarpine. Then they were divided into four groups: epilepsy model, VNS-treated, and sodium valproate-treated (VPA), and sham groups (<i>n</i> = 6/group). VNS was administered at parameters of 1 mA, 30 Hz, 250 μs pulse width, for 30 min/12 h. Cognitive function was assessed by the Morris water maze. Hippocampal neuronal damage, apoptosis and pathology were evaluated <i>via</i> Nissl, TUNEL and H&E staining, respectively. Oxidative stress markers were quantified by ELISA, while ROS were detected using DCFH-DA probes. Western blotting analyzed expression levels of Bcl-2, Bax, ERK, p-ERK, CREB, p-CREB and BDNF in the cerebral cortex.</p><p><strong>Results: </strong>Healthy rats exhibited abundant, evenly distributed Nissl bodies and orderly arranged cortical neurons. The epilepsy group showed cytoplasmic hypochromia and disorganized neuronal arrangement. VNS restored neuronal morphology to an extent comparable with VPA treatment. Compared to sham group, the epilepsy group demonstrated increased seizure frequency, duration, Racine scores, and escape latency, alongside reduced target quadrant occupancy. Elevated MDA, TNF-α and ROS levels were observed in the cerebral cortex, while SOD, IL-10, p-ERK/ERK, p-CREB/CREB and BDNF levels were reduced. VNS significantly ameliorated these pathological changes.</p><p><strong>Conclusion: </strong>VNS enhances cognitive function in epileptic rats, potentially through activation of the ERK/CREB/BDNF pathway in the cerebral cortex, thereby attenuating oxidative stress and neuroinflammation.</p>","PeriodicalId":14161,"journal":{"name":"International Journal of Neuroscience","volume":" ","pages":"1-11"},"PeriodicalIF":1.5,"publicationDate":"2025-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144775370","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":"Hippocampal neural stem cells in Alzheimer's disease: bridging neurogenesis, extracellular vesicles, and multimodal therapeutic paradigms.","authors":"Ruoyu Li, Wenrui Xiong, Chong Sun","doi":"10.1080/00207454.2025.2540989","DOIUrl":"https://doi.org/10.1080/00207454.2025.2540989","url":null,"abstract":"<p><p>Alzheimer's disease (AD) presents a formidable challenge in neurodegenerative medicine because of its complex pathophysiology and the absence of effective disease-modifying therapies. Emerging evidence suggests that impaired adult hippocampal neurogenesis (AHN), a dynamic process essential for cognitive plasticity, is a mechanistic contributor to AD progression. This review highlights the role of hippocampal neural stem cells (NSCs) in the pathogenesis of AD, including the molecular mechanisms underlying the neurogenic decline in AD and their potential impact on cognitive resilience. We summarize current therapeutic approaches, including pharmacological agents and non-pharmacological interventions (e.g. exercise, cognitive training, dietary strategies, and neurostimulation therapies), and explore their influence on neurogenesis. Additionally, we explore the potential application of NSCs in AD treatment, specifically through the use of NSC-derived extracellular vesicles (NSC-EVs) as a novel therapeutic modality. By integrating insights from AHN research and cutting-edge therapeutic advancements, this review emphasizes the therapeutic potential of promoting neurogenesis to address cognitive decline and advance treatment strategies for AD.</p>","PeriodicalId":14161,"journal":{"name":"International Journal of Neuroscience","volume":" ","pages":"1-21"},"PeriodicalIF":1.5,"publicationDate":"2025-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144799045","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":"Immunohistochemical characterisation of dopaminergic and cholinergic alterations in the prefrontal cortex and hippocampus of MPTP-treated marmosets.","authors":"Sanaa Khosla","doi":"10.1080/00207454.2025.2540288","DOIUrl":"https://doi.org/10.1080/00207454.2025.2540288","url":null,"abstract":"<p><p>Motor symptoms traditionally characterise Parkinson's disease (PD), but cognitive dysfunctions have recently emerged as significant non-motor features. While dopamine deficiency in the substantia nigra primarily causes PD, recent evidence indicates disruptions in neurochemical pathways beyond the nigrostriatal system also contribute to cognitive dysfunction. This preclinical study examines the roles of dopamine and acetylcholine (ACh) within the hippocampus and prefrontal cortex (PFC), assessing how their combined reduction manifests as neurochemical alterations in brain regions relevant to cognitive function in PD. Ten adult marmosets were used; five were treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to model Parkinsonian pathology, and five served as healthy controls. Immunohistochemistry (IHC) quantified critical changes using ImageJ software. Results indicated MPTP significantly reduced neuron count, fibre length and optical density (OD) in both regions. Specifically, tyrosine hydroxylase (TH)-positive neurons decreased by 66.2% in the hippocampus and 48.7% in the PFC, while choline acetyltransferase (ChAT)-positive neurons decreased by 47.6% and 39.5%, respectively. Fibre length and OD similarly decreased by more than 55% in both regions. These uniform neurochemical alterations provide insights into the multifactorial neurochemical pathology observed in brain regions associated with cognitive dysfunction in PD. Although behavioural assessments were not conducted, the observed histopathological alterations in this model correspond with established neural substrates implicated in PD-related cognitive dysfunction. These findings underscore the need for targeted therapeutic strategies that address the complex, multi-neurotransmitter basis of the neurochemical pathology associated with cognitive dysfunction in PD.</p>","PeriodicalId":14161,"journal":{"name":"International Journal of Neuroscience","volume":" ","pages":"1-9"},"PeriodicalIF":1.5,"publicationDate":"2025-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144799046","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":"Thymic stromal lymphopoietin modification gates chronic pain via regulation of transient receptor potential vanilloid type 1-caspase1.","authors":"Ying-Yi Lu, Chun-Ching Lu, Hung-Pei Tsai, Chieh-Hsin Wu","doi":"10.1080/00207454.2025.2541299","DOIUrl":"10.1080/00207454.2025.2541299","url":null,"abstract":"<p><strong>Aim: </strong>Given that depletion of thymic stromal lymphopoietin (TSLP) signals is a potential therapeutic option to relieve chronic pain, in this study, we aimed to explore the role of TSLP in regulation of chronic pain and clarify the interactions between TRPV1 and caspase1.</p><p><strong>Methods: </strong>Bleomycin (BLM), one derivative of <i>Streptomyces verticellus</i>, was administered into mouse to generate chronic mechanical pain in wild type (WT) mice and TSLP knockout mice. Four groups were divided including WT + saline, WT+BLM, TSLP knockout + saline and TSLP knockout + BLM. Differentiated SH-SY5Y cells were then established as a neuronal cell model. Pain behavioral test, cell viability test, western blot and immunofluorescence staining were used to evaluate the effects of <i>TSLP</i> depletion on glial reaction, neuronal death and inflammation.</p><p><strong>Results: </strong>Bleomycin enhanced the TRPV1-caspase1 signaling to induce chronic pain in mice. Compared to the mice receiving saline, glial reaction and neuronal death were augmented in the somatosensory cortex of the mice receiving bleomycin. In contrast, bleomycin also activated glial reaction and neuronal death in TSLP knockout mice but to a lower extent than those in WT mice with altered mechanical withdrawal threshold. In differentiated SH-SY5Y cells, silencing of <i>TSLP</i> decreased the expression of TRPV1-caspase1 as well as neuronal death induced by H<sub>2</sub>O<sub>2</sub>.</p><p><strong>Conclusions: </strong>By regulating glial reaction, neuronal death and inflammation, TSLP is a candidate target to treat chronic pain along with TRPV1-caspase1.</p>","PeriodicalId":14161,"journal":{"name":"International Journal of Neuroscience","volume":" ","pages":"1-9"},"PeriodicalIF":1.5,"publicationDate":"2025-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144775369","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 mitochondrial-derived peptide MOTS-c contributes to the protective effect against brain injury associated with LPS-induced sepsis by strengthening the blood-brain barrier's ultrastructure.","authors":"Yuanyuan Bai, Haiyan Wu, Xu Wang, Yang Guo, Bingqing Gong, Beibei Dong, Yonghao Yu","doi":"10.1080/00207454.2025.2542883","DOIUrl":"10.1080/00207454.2025.2542883","url":null,"abstract":"<p><strong>Background: </strong>Sepsis-associated encephalopathy (SAE) is a serious complication of sepsis, increasing short-term and long-term mortality. It involves neuroinflammation, neuronal damage, and blood-brain barrier (BBB) disruption. MOTS-c, a mitochondrion-derived peptide, exerts neuroprotective effects by modulating inflammatory responses and cellular functions. This study explored the protective effects of MOTS-c against brain injury in mice with LPS-induced sepsis.</p><p><strong>Methods: </strong>A mouse model of sepsis was established <i>via</i> intraperitoneal injection of LPS. The mice were divided into four groups: Control, Control + MOTS-c, LPS, and LPS + MOTS-c groups. The mice in the latter two groups received MOTS-c (20 mg/kg) four hours before model establishment. Survival rates and the murine sepsis score (MSS) were recorded. H&E staining, ELISA, Evans blue staining, brain water content detremination, immunofluorescence staining, western blotting, and qPCR were performed to assess brain tissue damage, inflammation, BBB permeability, and BBB-related protein expression.</p><p><strong>Results: </strong>MOTS-c treatment increased the survival rate, decreased the MSS score, alleviated brain tissue damage, downregulated the expression of inflammatory factors, reversed the increase in BBB permeability, upregulated the expression of BBB-related proteins and CD31/PDGFRβ, decreased the expression of GFAP/Iba-1/MMP-9, and increased the expression of neurotrophic factors in septic mice.</p><p><strong>Conclusion: </strong>MOTS-c effectively reduced mortality rates and the MSS, attenuated neuroinflammatory responses, mitigated increase in BBB permeability, promoted neurotrophic factor production, and protecting against brain injury in mice with LPS-induced sepsis.</p>","PeriodicalId":14161,"journal":{"name":"International Journal of Neuroscience","volume":" ","pages":"1-14"},"PeriodicalIF":1.5,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144768643","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}
Chawen Ding, Lei Zheng, Mingjian Xiong, Dongping Zhang, Zhongmei Chen, Linge Wang, Zhihua Luo, Hong Qiao
{"title":"Clinical and biochemical evaluation of rituximab as add on therapy in neuromyelitis optica spectrum disorders.","authors":"Chawen Ding, Lei Zheng, Mingjian Xiong, Dongping Zhang, Zhongmei Chen, Linge Wang, Zhihua Luo, Hong Qiao","doi":"10.1080/00207454.2024.2338255","DOIUrl":"10.1080/00207454.2024.2338255","url":null,"abstract":"<p><strong>Objective: </strong>This study assesses the efficacy of rituximab in the treatment of neuromyelitis optica spectrum disorders (NMOSD).</p><p><strong>Methods: </strong>The study initially included 40 patients with NMOSD diagnosed, after excluding patients who did not meet the complete inclusion criteria. Patients in the conventional group received routine clinical treatment, while patients in the study group received additional treatment with rituximab on the basis of the conventional treatment. Baseline data and clinically relevant indicators were collected for all patients, and the efficacy was compared between the two groups.</p><p><strong>Results: </strong>Baseline data were comparable between the two groups (<i>p</i> > 0.05). The EDSS scores after clinical treatment in the study group were lower than those in the conventional group, and the difference in EDSS scores before and after treatment was higher than that in the conventional group (<i>p</i> < 0.05). The difference in visual acuity correction before and after treatment was not significant between the two groups (<i>p</i> > 0.05). Laboratory indicators in the study group after clinical treatment were superior to those in the conventional group (all <i>p</i> < 0.05). The recurrence rate after clinical treatment in the study group was significantly lower than that in the conventional group (<i>p</i> < 0.05). Adverse reactions after clinical treatment in the study group were less than those in the conventional group (<i>p</i> < 0.05).</p><p><strong>Conclusion: </strong>This study found that rituximab demonstrated significant efficacy in the acute attacks and recurrence prevention of NMOSD, emphasizing its relatively good safety and tolerability. It highlights the potential of rituximab in treating NMOSD and provides valuable insights for future disease management.</p>","PeriodicalId":14161,"journal":{"name":"International Journal of Neuroscience","volume":" ","pages":"880-885"},"PeriodicalIF":1.5,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140335560","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":"The effect of the concurrent use of Dexmedetomidine (DEX) during the perioperative period on the renal function of patients following craniocerebral interventional surgery.","authors":"Lu Qian, Nianqiang Hu, Yijin Yu","doi":"10.1080/00207454.2024.2335530","DOIUrl":"10.1080/00207454.2024.2335530","url":null,"abstract":"<p><strong>Background: </strong>Craniocerebral interventional surgery is a common and essential treatment for cerebrovascular diseases. Despite continuous progress in interventional diagnosis and treatment technology, there is no effective method to alleviate contrast-induced kidney injuries. In this retrospective cohort study, we investigated the effect of the concurrent use of Dexmedetomidine (DEX) during the perioperative period on the renal function of patients following craniocerebral interventional surgery.</p><p><strong>Methods: </strong>We identified 228 cases of patients underwent craniocerebral interventional surgery from January 2018 to March 2022. Patients who used DEX during general anesthesia were in the DEX group (DEX group) or that did not use dexmedetomidine as the control group (CON group). The markers of kidney injury were recorded before and within 48 h after surgery.</p><p><strong>Results: </strong>Compared with CON group, the urea nitrogen (BUN) of the DEX group decreased significantly on the first day and the second day after surgery (<i>p</i> < 0.05). The serum cystatin-C and the blood urea nitrogen/creatinine ratio (BUN/Cr) was significantly lower than that in CON group on the second day (<i>p</i> < 0.05). The urine output in the DEX group increased significantly, and the mean arterial pressure (MAP) was higher than the CON group (<i>p</i> < 0.01). There was no difference in postoperative complications, ICU stay time and hospitalization time between the two groups.</p><p><strong>Conclusion: </strong>The combined use of dexmedetomidine in general anesthesia for craniocerebral interventional surgery can reduce BUN levels within 48 h after surgery, significantly increase intraoperative urine volume, maintain intraoperative circulation stability.</p>","PeriodicalId":14161,"journal":{"name":"International Journal of Neuroscience","volume":" ","pages":"851-862"},"PeriodicalIF":1.5,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140206840","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}