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Treadmill exercise improves hippocampal neural plasticity and relieves cognitive deficits in a mouse model of epilepsy

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Neural Regeneration Research 2024年第3期19卷 657-662页

作者： Hang Yu Mingting Shao Xi Luo Chaoqin Pang Kwok-Fai So Jiandong Yu Li Zhang Key Laboratory of CNS Regeneration(Ministry of Education) Guangdong-Hong Kong-Macao Institute of CNS RegenerationJinan UniversityGuangzhouGuangdong ProvinceChina State Key Laboratory of brain and Cognitive Science Li Ka Shing Faculty of MedicineThe University of Hong KongHong Kong Special Administrative RegionChina Neuroscience and Neurorehabilitation Institute University of Health and Rehabilitation SciencesQingdaoShandong ProvinceChina Department of Neurosurgery The First Affiliated Hospital of Bengbu Medical CollegeBengbuShandong ProvinceChina School of Psychology Shanghai University of SportShanghaiChina

Epilepsy frequently leads to cognitive dysfunction and approaches to treatment remain limited.Although regular exercise effectively improves learning and memory functions across multiple neurological diseases,its application in patients with epilepsy remains controversial.Here,we adopted a 14-day treadmill-exercise paradigm in a pilocarpine injection-induced mouse model of epilepsy.Cognitive assays confirmed the improvement of object and spatial memory after endurance training,and electrophysiological studies revealed the maintenance of hippocampal plasticity as a result of physical exercise.Investigations of the mechanisms underlying this effect revealed that exercise protected parvalbumin interneurons,probably via the suppression of neuroinflammation and improved integrity of blood-brain barrier.In summary,this work identified a previously unknown mechanism through which exercise improves cognitive rehabilitation in epilepsy.

关键词： blood-brain barrier cognition hippocampus interneurons long-term potentiation microglial cell neuroinflammation spatial memory temporal epilepsy treadmill exercise

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A novel FGFR1 inhibitor CYY292 suppresses tumor progression,invasion,and metastasis of glioblastoma by inhibiting the Akt/GSK3β/snail signaling axis

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Genes & Diseases 2024年第1期11卷 479-494页

作者： Yanran Bi Ruiling Zheng Jiahao Hu Ruiqing Shi Junfeng Shi Yutao Wang Peng Wang Wenyi Jiang Gyudong Kim Zhiguo Liu Xiaokun Li Li Lin School of Pharmaceutical Science Wenzhou Medical UniversityWenzhouZhejiang 325035China College of Pharmacy and Research Institute of Drug Development Chonnam National UniversityGwangju 61186Republic of Korea Department of Dermatology Wenzhou Hospital of Integrated Traditional Chinese and Western MedicineWenzhouZhejiang 325000China Zhejiang Lab for Regenerative Medicine Oujiang LaboratoryWenzhouZhejiang 325035China

Glioblastoma(GBM)is a malignant brain tumor that grows quickly,spreads widely,and is resistant to treatment.Fibroblast growth factor receptor(FGFR)1 is a receptor tyrosine kinase that regulates cellular processes,including proliferation,survival,migration,and dif-ferentiation.FGFR1 was predominantly expressed in GBM tissues,and FGFR1 expression was negatively correlated with overall survival.We rationally designed a novel small molecule CYY292,which exhibited a strong affinity for the FGFR1 protein in GBM cell lines in vitro.CYY292 also exerted an effect on the conserved Ser777 residue of FGFR1.CYY292 dose-depen-dently inhibited cell proliferation,epithelial-mesenchymal transition,stemness,invasion,and migration in vitro by specifically targeting the FGFR1/AKT/Snail pathways in GBM cells,and this effect was prevented by pharmacological inhibitors and critical gene knockdown.In vivo experiments revealed that CYY292 inhibited U87MG tumor growth more effectively than AZD4547.CYY292 also efficiently reduced GBM cell proliferation and increased survival in orthotopic GBM models.This study further elucidates the function of FGFR1 in the GBM and reveals the effect of CYY292,which targets FGFR1,on downstream signaling pathways directly reducing GBM cell growth,invasion,and metastasis and thus impairing the recruitment,activation,and function of immune cells.

关键词： blood-brain barrier EMT FGFR1 FGFR1 inhibitor Glioblastoma

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Biomaterials-based anti-inflammatory treatment strategies for Alzheimer's disease

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Neural Regeneration Research 2024年第1期19卷 100-115页

作者： Jianjian Chu Weicong Zhang Yan Liu Baofeng Gong Wenbo Ji Tong Yin Chao Gao Danqi Liangwen Mengqi Hao Cuimin Chen Jianhua Zhuang Jie Gao You Yin Department of Neurology Second Affiliated Hospital(Shanghai Changzheng Hospital)of Naval Medical UniversityShanghaiChina School of Pharmacy University College LondonLondonUK Department of Clinical Pharmacy Xinhua HospitalShanghai Jiao Tong University School of MedicineClinical Pharmacy Innovation InstituteShanghai Jiao Tong University School of MedicineShanghaiChina School of Health Science and Engineering University of Shanghai for Science and TechnologyShanghaiChina Changhai Clinical Research Unit Shanghai Changhai HospitalNaval Medical UniversityShanghaiChina

The current therapeutic drugs for Alzheimer's disease only improve symptoms,they do not delay disease progression.Therefo re,there is an urgent need for new effective drugs.The underlying pathogenic factors of Alzheimer's disease are not clear,but neuroinflammation can link various hypotheses of Alzheimer's disease;hence,targeting neuroinflammation may be a new hope for Alzheimer's disease treatment.Inhibiting inflammation can restore neuronal function,promote neuro regeneration,reduce the pathological burden of Alzheimer's disease,and improve or even reverse symptoms of Alzheimer's disease.This review focuses on the relationship between inflammation and various pathological hypotheses of Alzheimer's disease;reports the mechanisms and characteristics of small-molecule drugs(e.g.,nonsteroidal anti-inflammatory drugs,neurosteroids,and plant extracts);macromolecule drugs(e.g.,peptides,proteins,and gene therapeutics);and nanocarriers(e.g.,lipid-based nanoparticles,polymeric nanoparticles,nanoemulsions,and inorganic nanoparticles)in the treatment of Alzheimer's disease.The review also makes recommendations for the prospective development of anti-inflammatory strategies based on nanocarriers for the treatment of Alzheimer's disease.

关键词： Alzheimer's disease anti-inflammation blood-brain barrier drug delivery microglia nanoparticles neuroinflammation plant extracts

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Advanced nano drug delivery systems for neuroprotection against ischemic stroke

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Chinese Chemical Letters 2024年第2期35卷 151-162页

作者： Chenchen Xie Jun Liao Ning Zhang Yuhan Sun Yi Li Liyan Xiong Yingnan Zhang Xiaoyan Liu Wei Su Heming Chen Ping Zeng Xiaoqing Zhang Ying Lu Tingfang Wang Chuan Zhang Shanghai Engineering Research Center of Organ Repair School of MedicineShanghai UniversityShanghai 200444China Department of Pharmaceutical Science School of PharmacyNaval Medical UniversityShanghai 200433China Department of pharmacy the International Peace Maternity and Child Health HospitalSchool of MedicineShanghai Jiao Tong UniversityShanghai 200030China School of Pharmacy Shanghai Jiao Tong UniversityShanghai 200040China

Ischemic stroke(IS)represents a significant threat to brain health due to its elevated mortality and disability rates.The efficacy of small-molecule neuroprotective agents has been impeded by challenges associated with traversing the blood-brain barrier(BBB)and limited bioavailability.Conversely,advanced nano drug delivery systems hold promise for overcoming these obstacles by facilitating efficient transportation across the BBB and maintaining optimal drug concentrations.This review aims to explore advanced neuroprotective nano drug delivery systems as a means of effectively administering neuroprotective agents to the brain using pharmaceutical approaches in the treatment of IS.By examining these systems,researchers and clinicians can gain valuable insights and innovative concepts,illuminating the potential of advanced neuroprotective nano drug delivery systems.Leveraging these advancements can drive the progress of pioneering and efficacious therapeutic interventions for IS.

关键词： Target blood-brain barrier Ischemic stroke Nano drug delivery Neuroprotection

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Perihematomal endothelin-1 level is associated with an increase in blood-brain barrier permeability in a rabbit model of intracerebral hematoma

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Chinese Medical Journal 2013年第18期126卷 3433-3438页

作者： WANG Li-kun HONG Zhen WU Guo-feng LI Chang Department of Neurology Affiliated Huashan Hospital of Fudan University Shanghai 200036 China Department of Neurology Affiliated Hospital of Guiyang Medical University Guiyang Guizhou 550004 China

Background Endothelin-1 （ET-1） has deleterious effects on water homeostasis, cerebral edema, and blood-brain barrier （BBB） integrity. Highly expressed ET-1 was observed after intracerebral hemorrhage （ICH）; however, ET-1 changes and their relationship with BBB disruption within 24 hours of ICH have not been thoroughly investigated. The aim of the present study was to observe the changes in perihematomal ET-1 levels in various phases of ICH and their correlation with the BBB integrity in a rabbit model of ICH. Methods Twenty-five rabbits （3.2-4.3 kg body weight） were randomly divided into a normal control group （five rabbits） and a model group （20 rabbits）. Animals in the model group were equally divided into four subgroups （five rabbits each to be sacrificed at 6, 12, 18, and 24 hours following ICH establishment）. An ICH model was prepared in the model group by infusing autologous arterial blood into the rabbit brain. ET-1 expression in perihematomal brain tissues was determined using immunohistochemistry and color image analysis, and the permeability of the BBB was assayed using the Evan＇s Blue （EB） method. A repeated measures analysis of variance was used to make comparisons of the ET-1 and EB content across the entire time series. Results The number of perihematomal endothelial cells with ET-1 positive expressions following 6, 12, 18, and 24 hours ICH model establishment was 9.32, 13.05, 15.90, and 20.44, respectively, but as low as 6.67 in the control group. The average transmittance of ET-1-positive cell bodies at 6, 12, 18, and 24 hours after ICH was 99.10, 97.40, 85.70, and 80.80, respectively, but 100.12 in the control group. These data reveal that the expression of ET-1 was significantly increased at 6, 12, 18, and 24 hours after ICH compared with the control group, and a marked decrease in the average transmittance of ET-l-positive cell bodies was noted （P 〈0.05）. Similarly, the perihematomal EB content at 6, 12, 18, and 24 hours after ICH was 29.39±1.16, 32.20±0.73, 33.63±1.08, and 35.26±1.12, respecti

关键词： intracerebral hemorrhage endothelin-1 blood-brain barrier Evan＇s blue brain edema

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Mechanisms of imperatorin on regulating Pglycoprotein in blood-brain barrier based on network pharmacology and in vitro experiment

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中国药理学与毒理学杂志 2023年第S1期37卷 17-18页

作者： SONG Yizhen YIN Wanxin MA Yicong AN Yufan HUANG Jiaqi YAN Zhongjie WU Xiuwen WANG Yuanyu School of Pharmaceutical Sciences Hebei Medical UniversityShijiazhuang 050017China Department of Neurosurgery the Second Hospital of Hebei Medical UniversityShijiazhuang 050000China

OBJECTIVE To explore mecha⁃nisms of imperatorin on regulating P-glycoprotein(P-gp)in blood-brain barrier(BBB)based on net⁃work pharmacology combined with in vitro experi⁃ment.METHODS Drug targets were predicted using the Pharmapper and Swiss targets data⁃bases;disease targets were obtained through the Genecards database;intersections between drugs and disease targets were screened by Cytoscape software;the obtained core targets were used to construct protein-protein interaction(PPI)network,gene ontology(GO)functions,and Kyoto encyclopedia of genes and genomes(KEGG)pathway enrichment analysis.The effects of imperatorin(20,50,100μmol·L^(-1))on P-gp activity were monitored in hCMEC/D3 in vitro BBB model,and the effects of imperatorin on the expression of target proteins were verified using Western blot method.RESULTS 55 drug targets and 3102 disease targets were obtained from the network pharmacology screening,and 37 core targets were obtained after the combination.Enrichment analysis showed that core targets were closely related to chemical synaptic trans⁃mission regulation,neurotransmitter receptor activity,protein kinase regulation activity,G proteincoupled receptor signaling pathway,neural active ligand receptor interaction pathway,PI3K-Akt sig⁃naling pathway,VEGF signaling pathway,etc..In vitro experimental validation suggested that all tested concentration groups of imperatorin signifi⁃cantly reduced the activity and expression of P-gp,which were achieved by significantly downregu⁃lating the phosphorylation levels of PI3K and Akt,and repressing the expression of VEGFR2 pro⁃tein.CONCLUSION Network pharmacology was used to predict the core targets and signaling pathways of imperatorin on regulating P-gp in BBB and relevant validation was conducted through in vitro experiments,providing a refer⁃ence basis for further exploration of the mecha⁃nisms of imperatorin on regulating P-gp in BBB.

关键词： imperatorin blood-brain barrier P-glycoprotein network pharmacology in vitro experiment

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Aloin Protects Against blood-brain barrier Damage After Traumatic brain Injury in Mice

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Neuroscience Bulletin 2020年第6期36卷 625-638页

作者： Yao Jing Dian-Xu Yang Wei Wang Fang Yuan Hao Chen Jun Ding Zhi Geng Heng-Li Tian Department of Neurosurgery Shanghai Jiao Tong University Affiliated Sixth People's HospitalShanghai 200233China Department of Neurology Shanghai Jiao Tong University Affiliated Sixth People’s HospitalShanghai 200233China

Aloin is a small-molecule drug well known for its protective actions in various models of damage.Traumatic brain injury(TBI)-induced cerebral edema from secondary damage caused by disruption of the blood-brain barrier(BBB) often leads to an adverse prognosis.Since the role of aloin in maintaining the integrity of the BBB after TBI remains unclear,we explored the protective effects of aloin on the BBB using in vivo and in vitro TBI models.Adult male C57 BL/6 mice underwent controlled cortical impact injury,and mouse brain capillary endothelial bEnd.3 cells underwent biaxial stretch injury,then both received aloin treatment.In the animal experiments,we found 20 mg/kg aloin to be the optimum concentration to decrease cerebral edema,decrease disruption of the BBB,and improve neurobehavioral performance after cortical impact injury.In the cellular studies,the optimum concentration of 40 μg/mL aloin reduced apoptosis and reversed the loss of tight junctions by reducing the reactive oxygen species levels and changes in mitochondrial membrane potential after stretch injury.The mechanisms may be that aloin downregulates the phosphorylation of p38 mitogen-activated protein kinase,the activation of p65 nuclear factor-kappa B,and the ratios of B cell lymphoma(Bcl)-2-associated X protein/Bcl-2 and cleaved caspase-3/caspase-3.We conclude that aloin exhibits these protective effects on the BBB after TBI through its anti-oxidative stress and anti-apoptotic properties in mouse brain capillary endothelial cells.Aloin may thus be a promising therapeutic drug for TBI.

关键词： Aloin blood-brain barrier Traumatic brain injury Oxidative stress Apoptosis

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The blood–brain barrier in systemic infection and inflammation

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Cellular & Molecular Immunology 2021年第11期18卷 2489-2501页

作者： Ian Galea Clinical Neurosciences Clinical&Experimental SciencesFaculty of MedicineUniversity of SouthamptonSouthamptonSO166YDUK

The vascular blood-brain barrier is a highly regulated interface between the blood and brain.Its primary function is to protect central neurons while signaling the presence of systemic inflammation and infection to the brain to enable a protective sickness behavior response.With increasing degrees and duration of systemic inflammation,the vascular blood-brain barrier becomes more permeable to solutes,undergoes an increase in lymphocyte trafficking,and is infiltrated by innate immune cells;endothelial cell damage may occasionally occur.Perturbation of neuronal function results in the clinical features of encephalopathy.Here,the molecular and cellular anatomy of the vascular blood-brain barrier is reviewed,first in a healthy context and second in a systemic inflammatory context.Distinct from the molecular and cellular mediators of the blood-brain barrier’s response to inflammation,several moderators influence the direction and magnitude at genetic,system,cellular and molecular levels.These include sex,genetic background,age,pre-existing brain pathology,systemic comorbidity,and gut dysbiosis.Further progress is required to define and measure mediators and moderators of the blood-brain barrier’s response to systemic inflammation in order to explain the heterogeneity observed in animal and human studies.

关键词： blood-brain barrier inflammation infection signaling moderation

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Hyperoside protects the blood-brain barrier from neurotoxicity of amyloid beta 1–42

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Neural Regeneration Research 2018年第11期13卷 1974-1980页

作者： Chen-Yang Liu Kuan Bai Xiao-Hui Liu Li-Mi Zhang Gu-Ran Yu Department of Neurology Jiangsu Traditional Chinese Medicine Hospital the Affiliated Hospital of Nanjing University of Traditional Chinese Medicine Nanjing Jiangsu Province China Graduate School of Nanjing University of Traditional Chinese Medicine Nanjing Jiangsu Province China

Mounting evidence indicates that amyloid β protein（Aβ） exerts neurotoxicity by disrupting the blood-brain barrier（BBB） in Alzheimer＇s disease. Hyperoside has neuroprotective effects both in vitro and in vivo against Aβ. Our previous study found that hyperoside suppressed Aβ1-42-induced leakage of the BBB, however, the mechanism remains unclear. In this study, bEnd.3 cells were pretreated with 50, 200, or 500 μM hyperoside for 2 hours, and then exposed to Aβ1-42 for 24 hours. Cell viability was determined using 3-（4,5-dimethyl-2-thiazolyl）-2,5-diphenyl-2-H-tetrazolium bromide assay. Flow cytometry and terminal deoxynucleotidyl transferase-mediated d UTP nick-end labeling assay were used to analyze cell apoptosis. Western blot assay was carried out to analyze expression levels of Bax, Bcl-2, cytochrome c, caspase-3, caspse-8, caspase-9, caspase-12, occludin, claudin-5, zonula occludens-1, matrix metalloproteinase-2（MMP-2）, and MMP-9. Exposure to Aβ1-42 alone remarkably induced bEnd.3 cell apoptosis; increased ratios of cleaved caspase-9/caspase-9, Bax/Bcl-2, cleav ed caspase-8/caspase-8, and cleaved caspase-12/caspase-12; increased expression of cytochrome c and activity of caspase-3; diminished levels of zonula occludens-1, claudin-5, and occludin; and increased levels of MMP-2 and MMP-9. However, hyperoside pretreatment reversed these changes in a dose-dependent manner. Our findings confirm that hyperoside alleviates fibrillar Aβ1-42-induced BBB disruption, thus offering a feasible therapeutic application in Alzheimer＇s disease.

关键词： nerve regeneration Alzheimer＇s disease amyloid beta 1-42 blood-brain barrier bEnd.3 cells tight junction proteins hyperoside anti-apoptosis neural regeneration

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Novel drug-delivery approaches to the blood-brain barrier

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Neuroscience Bulletin 2015年第2期31卷 257-264页

作者： Xiaoqing Wang Xiaowen Yu William Vaughan Mingyuan Liu Yangtai Guan Department of Neurology Changhai Hospital Second Military Medical University Stem Cells and Medical Research Center Second Military Medical University Department of Gerontology Changhai Hospital Second Military Medical University Department of Genetics Yale University

The blood-brain barrier （BBB） maintains homeostasis by blocking toxic molecules from the circulation, but drugs are blocked at the same time. When the dose is increased to enhance the drug concentration in the central nervous system, there are side-effects on peripheral organs. In recent years, genetic therapeutic agents and small molecules have been used in various strategies to penetrate the BBB while minimizing the damage to systemic organs. In this review, we describe several representative methods to circumvent or cross the BBB, including chemical and physical strategies.

关键词： drug delivery blood-brain barrier nanoparticles focused ultrasound

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