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Post-acute ischemic stroke hyperglycemia aggravates destruction of the blood-brain barrier

Neural Regeneration Research 2024年第6期19卷 1344-1350页

作者： Tianqi Xu Jianhong Yang Yao Xu Xiaofeng Wang Xiang Gao Jie Sun Chenhui Zhou Yi Huang Department of Neurology The First Affiliated Hospital of Ningbo University Department of General Surgery The First Affiliated Hospital of Ningbo University Department of Neurosurgery The First Affiliated Hospital of Ningbo University Key Laboratory of Precision Medicine for Atherosclerotic Diseases of Zhejiang Province

Post-acute ischemic stroke hyperglycemia increases the risk of hemorrhagic transformation, which is associated with blood-brain barrier disruption. brain microvascular endothelial cells are a major component of the blood-brain barrier. Intercellular mitochondrial transfer has emerged as a novel paradigm for repairing cells with mitochondrial dysfunction. In this study, we first investigated whether mitochondrial transfer exists between brain microvascular endothelial cells, and then investigated the effects of post-acute ischemic stroke hyperglycemia on mitochondrial transfer between brain microvascular endothelial cells. We found that healthy brain microvascular endothelial cells can transfer intact mitochondria to oxygen glucose deprivation-injured brain microvascular endothelial cells. However, post-oxygen glucose deprivation hyperglycemia hindered mitochondrial transfer and exacerbated mitochondrial dysfunction. We established an in vitro brain microvascular endothelial cell model of the blood-brain barrier. We found that post-acute ischemic stroke hyperglycemia reduced the overall energy metabolism levels of brain microvascular endothelial cells and increased permeability of the blood-brain barrier. In a clinical study, we retrospectively analyzed the relationship between post-acute ischemic stroke hyperglycemia and the severity of hemorrhagic transformation. We found that post-acute ischemic stroke hyperglycemia serves as an independent predictor of severe hemorrhagic transformation. These findings suggest that post-acute ischemic stroke hyperglycemia can aggravate disruption of the blood-brain barrier by inhibiting mitochondrial transfer.

关键词： acute ischemic stroke blood-brain barrier brain microvascular endothelial cells mitochondrial transfer stress hyperglycemia

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Targeting the blood-brain barrier to delay aging-accompanied neurological diseases by modulating gut microbiota,circadian rhythms,and their interplays

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Acta Pharmaceutica Sinica B 2023年第12期13卷 4667-4687页

作者： Yanping Wang Weihong Du Xiaoyan Hu Xin Yu Chun Guo Xinchun Jin Wei Wang Department of Neurology the Second Affliated Hospital of Jiaxing CityJiaxing 314000China Beijing Key Laboratory of Cancer Invasion and Metastasis Research Department of Histology and EmbryologySchool of Basic Medical SciencesAdvanced Innovation Center for Human Brain ProtectionCapital Medical UniversityBeijing 100069China Bengbu Medical College(Department of Neurology the Second Hospital of Jiaxing City)Jiaxing 233030China School of Biosciences University of SheffieldSheffeld S102TNUK Department of Physiology and Pathophysiology Capital Medical UniversityBeijing 100069China

AbstracTthe blood-brain barrier(BBB)impairment plays a crucial role in the pathological processes of aging-accompanied neurological diseases(AAND).Meanwhile,circadian rhythms disruption and gut microbiota dysbiosis are associated with increased morbidity of neurological diseases in the accelerated aging population.Importantly,circadian rhythms disruption and gut microbiota dysbiosis are also known to induce the generation of toxic metabolites and pro-inflammatory cytokines,resulting in disruption of BBB integrity.Collectively,this provides a new perspective for exploring the relationship among circadian rhythms,gut microbes,and the BBB in aging-accompanied neurological diseases.In this review,we focus on recent advances in the interplay between circadian rhythm disturbances and gut microbiota dysbiosis,and their potential roles in the BBB disruption that occurs in AAND.Based on existing literature,we discuss and propose potential mechanisms underlying BBB damage induced by dysregulated circadian rhythms and gut microbiota,which would serve as the basis for developing potential interventions to protect the BBB in the aging population through targeting the BBB by exploiting its links with gut microbiota and circadian rhythms for treating AAND.

关键词： blood-brain barrier Neurological diseases Aging Gut microbiota Circadian rhythms

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The role of fibronectin in multiple sclerosis and the effect of drug delivery across the blood-brain barrier

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Neural Regeneration Research 2023年第10期18卷 2147-2155页

作者： Shuang-Shuang Wei Le Chen Feng-Yuan Yang Si-Qi Wang Peng Wang Ningxia Key Laboratory of Craniocerebral Diseases School of Clinical MedicineNingxia Medical UniversityYinchuanNingxia Hui Autonomous RegionChina Ningxia Key Laboratory of Craniocerebral Diseases Ningxia Medical UniversityYinchuanNingxia Hui Autonomous RegionChina

Remyelination failure is one of the main characteristics of multiple sclerosis and is potentially correlated with disease progression.Previous research has shown that the extracellular matrix is associated with remyelination failure because remodeling of the matrix often fails in both chronic and progressive multiple sclerosis.Fibronectin aggregates are assembled and persistently exist in chronic multiple sclerosis,thus inhibiting remyelination.Although many advances have been made in the mechanisms and treatment of multiple sclerosis,it remains very difficult for drugs to reach pathological brain tissues;this is due to the complexity of brain structure and function,especially the existence of the blood-brain barrier.Therefore,herein,we review the effects of fibronectin aggregates on multiple sclerosis and the efficacy of different forms of drug delivery across the blood-brain barrier in the treatment of this disease.

关键词： blood-brain barrier brain delivery exosomes extracellular matrix fibronectin aggregates fibronectin intestinal flora multiple sclerosis remyelination failure remyelination

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Targeting brain tumors with innovative nanocarriers:bridging the gap through the blood-brain barrier

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Oncology Research 2024年第5期32卷 877-897页

作者： KARAN WADHWA PAYAL CHAUHAN SHOBHIT KUMAR RAKESH PAHWA RAVINDER VERMA RAJAT GOYAL GOVIND SINGH ARCHANA SHARMA NEHA RAO DEEPAK KAUSHIK Department of Pharmaceutical Sciences Maharshi Dayanand UniversityRohtak124001India Department of Pharmaceutical Technology Meerut Institute of Engineering and Technology(MIET)NH-58Delhi-Roorkee HighwayMeerut250005India Institute of Pharmaceutical Sciences Kurukshetra UniversityKurukshetra136119India Department of Pharmaceutical Sciences Chaudhary Bansi Lal UniversityBhiwani127021India MM College of Pharmacy Maharishi Markandeshwar(Deemed to be University)Mullana-AmbalaHaryana133207India Delhi Pharmaceutical Sciences and Research University(DIPSAR) Delhi Pharmaceutical Sciences and Research UniversityNew Delhi110017India

Background:Glioblastoma multiforme(GBM)is recognized as the most lethal and most highly invasive tumor.The high likelihood of treatment failure arises fromthe presence of the blood-brain barrier(BBB)and stemcells around GBM,which avert the entry of chemotherapeutic drugs into the tumormass.Objective:Recently,several researchers have designed novel nanocarrier systems like liposomes,dendrimers,metallic nanoparticles,nanodiamonds,and nanorobot approaches,allowing drugs to infiltrate the BBB more efficiently,opening up innovative avenues to prevail over therapy problems and radiation therapy.Methods:Relevant literature for this manuscript has been collected from a comprehensive and systematic search of databases,for example,PubMed,Science Direct,Google Scholar,and others,using specific keyword combinations,including“glioblastoma,”“brain tumor,”“nanocarriers,”and several others.Conclusion:This review also provides deep insights into recent advancements in nanocarrier-based formulations and technologies for GBM management.Elucidation of various scientific advances in conjunction with encouraging findings concerning the future perspectives and challenges of nanocarriers for effective brain tumor management has also been discussed.

关键词： Glioblastoma brain tumor blood-brain barrier Liposomes Metallic nanoparticles Nanocarriers

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Anti-Parkinsonian Therapy:Strategies for Crossing the blood–brain barrier and Nano-Biological Effects of Nanomaterials

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Nano-Micro Letters 2022年第6期14卷 350-398页

作者： Guowang Cheng Yujing Liu Rui Ma Guopan Cheng Yucheng Guan Xiaojia Chen Zhenfeng Wu Tongkai Chen Key Laboratory of Modern Preparation of Traditional Chinese Medicine Ministry of EducationJiangxi University of Chinese MedicineNanchang 330004People’s Republic of China Science and Technology Innovation Center Guangzhou University of Chinese MedicineGuangzhou 510405People’s Republic of China State Key Laboratory of Quality Research in Chinese Medicine Institute of Chinese Medical SciencesUniversity of MacaoMacao 999078People’s Republic of China

Parkinson’s disease(PD),a neurodegenerative disease that shows a high incidence in older individuals,is becoming increasingly prevalent.Unfortunately,there is no clinical cure for PD,and novel anti-PD drugs are therefore urgently required.However,the selective permeability of the blood–brain barrier(BBB)poses a huge challenge in the development of such drugs.Fortunately,through strategies based on the physiological characteristics of the BBB and other modifications,including enhancement of BBB permeability,nanotechnology can offer a solution to this problem and facilitate drug delivery across the BBB.Although nanomaterials are often used as carriers for PD treatment,their biological activity is ignored.Several studies in recent years have shown that nanomaterials can improve PD symptoms via their own nano-bio effects.In this review,we first summarize the physiological features of the BBB and then discuss the design of appropriate brain-targeted delivery nanoplatforms for PD treatment.Subsequently,we highlight the emerging strategies for crossing the BBB and the development of novel nanomaterials with anti-PD nano-biological effects.Finally,we discuss the current challenges in nanomaterial-based PD treatment and the future trends in this field.Our review emphasizes the clinical value of nanotechnology in PD treatment based on recent patents and could guide researchers working in this area in the future.

关键词： blood-brain barrier Parkinson’s disease Nasal delivery Biomimetic drug delivery Nano-biological effects

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Urolithin A alleviates blood-brain barrier disruption and attenuates neuronal apoptosis following traumatic brain injury in mice

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Neural Regeneration Research 2022年第9期17卷 2007-2013页

作者： Qiu-Yuan Gong Lin Cai Yao Jing Wei Wang Dian-Xu Yang Shi-Wen Chen Heng-Li Tian Department of Neurosurgery Shanghai Jiao Tong University Affiliated Sixth People’s HospitalShanghaiChina

Urolithin A(UA)is a natural metabolite produced from polyphenolics in foods such as pomegranates,berries,and nuts.UA is neuroprotective against Parkinson’s disease,Alzheimer’s disease,and cerebral hemorrhage.However,its effect against traumatic brain injury remains unknown.In this study,we established adult C57BL/6J mouse models of traumatic brain injury by controlled cortical impact and then intraperitoneally administered UA.We found that UA greatly reduced brain edema;increased the expression of tight junction proteins in injured cortex;increased the immunopositivity of two neuronal autophagy markers,microtubule-associated protein 1A/B light chain 3A/B(LC3)and p62;downregulated protein kinase B(Akt)and mammalian target of rapamycin(mTOR),two regulators of the phosphatidylinositol 3-kinase(PI3K)/Akt/mTOR signaling pathway;decreased the phosphorylation levels of inhibitor of NFκB(IκB)kinase alpha(IKKα)and nuclear factor kappa B(NFκB),two regulators of the neuroinflammation-related Akt/IKK/NFκB signaling pathway;reduced blood-brain barrier permeability and neuronal apoptosis in injured cortex;and improved mouse neurological function.These findings suggest that UA may be a candidate drug for the treatment of traumatic brain injury,and its neuroprotective effects may be mediated by inhibition of the PI3K/Akt/mTOR and Akt/IKK/NFκB signaling pathways,thus reducing neuroinflammation and enhancing autophagy.

关键词： autophagy blood-brain barrier cerebral edema controlled cortical impact model neuronal apoptosis neuropharmacology neuroprotection tight junction protein traumatic brain injury urolithin A

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Emerging roles of astrocytes in blood-brain barrier disruption upon amyloid-beta insults in Alzheimer's disease

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Neural Regeneration Research 2023年第9期18卷 1890-1902页

作者： Qian Yue Maggie Pui Man Hoi State Key Laboratory of Quality Research in Chinese Medicine Institute of Chinese Medical SciencesUniversity of MacaoMacao Special Administrative RegionChina Department of Pharmaceutical Sciences Faculty of Health SciencesUniversity of MacaoMacao Special Administrative RegionChina

blood-brain barrier disruption occurs in the early stages of Alzheimer’s disease.Recent studies indicate a link between blood-brain barrier dysfunction and cognitive decline and might accelerate Alzheimer’s disease progression.Astrocytes are the most abundant glial cells in the central nervous system with important roles in the structural and functional maintenance of the blood-brain barrier.For example,astrocytic cove rage around endothelial cells with perivascular endfeet and secretion of homeostatic soluble factors are two major underlying mechanisms of astrocytic physiological functions.Astrocyte activation is often observed in Alzheimer’s disease patients,with astrocytes expressing a high level of glial fibrillary acid protein detected around amyloid-beta plaque with the elevated phagocytic ability for amyloid-beta.Structural alte rations in Alzheimer’s disease astrocytes including swollen endfeet,somata shrinkage and possess loss contribute to disruption in vascular integrity at capillary and arte rioles levels.In addition,Alzheimer’s disease astrocytes are skewed into proinflammatory and oxidative profiles with increased secretions of vasoactive mediators inducing endothelial junction disruption and immune cell infiltration.In this review,we summarize the findings of existing literature on the relevance of astrocyte alte ration in response to amyloid pathology in the context of blood-brain barrier dysfunction.First,we briefly describe the physiological roles of astrocytes in blood-brain barrier maintenance.Then,we review the clinical evidence of astrocyte pathology in Alzheimer’s disease patients and the preclinical evidence in animal and cellular models.We further discuss the structural changes of blood-brain barrier that correlates with Alzheimer’s disease astrocyte.Finally,we evaluate the roles of soluble factors secreted by Alzheimer’s disease astrocytes,providing potential molecular mechanisms underlying blood-brain barrier modulation.We conclude with a perspective on investigating the therapeutic pot

关键词： Alzheimer’s disease amyloid-beta astrocyte(astroglial)-endothelial interaction astrocyte pathology blood-brain barrier blood-brain barrier disruption brain endothelial cell neuroinflammation reactive astrocyte

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CircLphn3 protects the blood-brain barrier in traumatic brain injury

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Neural Regeneration Research 2022年第4期17卷 812-818页

作者： Yu-Qi Cheng Chen-Rui Wu Meng-Ran Du Qiang Zhou Bi-Ying Wu Jia-Yuan-Yuan Fu Ehab Balawi Wei-Lin Tan Zheng-Bu Liao Department of Neurosurgery The First Affiliated Hospital of Chongqing Medical UniversityChongqingChina

Circular RNAs(circRNAs)are a new and large group of non-coding RNA molecules that are abundantly expressed in the central nervous system.However,very little is known about their roles in traumatic brain injury.In this study,we firstly screened differentially expressed circ RNAs in normal and injured brain tissues of mice after traumatic brain injury.We found that the expression of circ Lphn3 was substantially decreased in mouse models of traumatic brain injury and in hemin-treated b End.3(mouse brain cell line)cells.After overexpressing circ Lphn3 in b End.3 cells,the expression of the tight junction proteins,ZO-1,ZO-2,and occludin,was upregulated,and the expression of mi R-185-5 p was decreased.In b End.3 cells transfected with mi R-185-5 p mimics,the expression of ZO-1 was decreased.Dual-luciferase reporter assays showed that circ Lphn3 bound to mi R-185-5 p,and that mi R-185-5 p bound to ZO-1.Additionally,circ Lphn3 overexpression attenuated the hemin-induced high permeability of the in vitro b End.3 cell model of the blood-brain barrier,while mi R-185-5 p transfection increased the permeability.These findings suggest that circ Lphn3,as a molecular sponge of mi R-185-5 p,regulates tight junction proteins'expression after traumatic brain injury,and it thereby improves the permeability of the blood-brain barrier.This study was approved by the Animal Care and Use Committee of Chongqing Medical University of China(approval No.2021-177)on March 22,2021.

关键词： bioinformatics blood-brain barrier circ RNA mi RNA RNA-sequence tight junction protein traumatic brain injury ZO1

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Sphingosine 1-phosphate receptor 1 regulates bloodbrain barrier permeability in epileptic mice

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Neural Regeneration Research 2023年第8期18卷 1763-1769页

作者： Li-Xiang Yang Yuan-Yuan Yao Jiu-Rong Yang Hui-Lin Cheng Xin-Jian Zhu Zhi-Jun Zhang Department of Neurosurgery Zhongda HospitalSchool of MedicineSoutheast UniversityNanjingJiangsu ProvinceChina Department of Pharmacology Medical School of Southeast UniversityNanjingJiangsu ProvinceChina Department of Neurology Zhongda HospitalSchool of MedicineInstitution of NeuropsychiatryKey Laboratory of Developmental Genes and Human DiseaseSoutheast UniversityNanjingJiangsu ProvinceChina Department of Mental Health and Public Health Faculty of Life and Health SciencesShenzhen Institute of Advanced TechnologyChinese Academy of SciencesShenzhenGuangdong ProvinceChina

Destruction of the blood-brain barrier is a critical component of epilepsy pathology.Several studies have demonstrated that sphingosine 1-phosphate receptor 1 contributes to the modulation of vascular integrity.However,its effect on blood-brain barrier permeability in epileptic mice remains unclear.In this study,we prepared pilocarpine-induced status epilepticus models and pentylenetetrazol-induced epilepsy models in C57BL/6 mice.S1P1 expression was increased in the hippocampus after status epilepticus,whereas tight junction protein expression was decreased in epileptic mice compared with controls.Intraperitoneal injection of SEW2871,a specific agonist of sphingosine-1-phosphate receptor 1,decreased the level of tight junction protein in the hippocampus of epileptic mice,increased blood-brain barrier leakage,and aggravated the severity of seizures compared with the control.W146,a specific antagonist of sphingosine-1-phosphate receptor 1,increased the level of tight junction protein,attenuated blood-brain barrier disruption,and reduced seizure severity compared with the control.Furthermore,sphingosine 1-phosphate receptor 1 promoted the generation of interleukin-1βand tumor necrosis factor-αand caused astrocytosis.Disruption of tight junction protein and blood-brain barrier integrity by sphingosine 1-phosphate receptor 1 was reversed by minocycline,a neuroinflammation inhibitor.Behavioral tests revealed that sphingosine 1-phosphate receptor 1 exacerbated epilepsy-associated depression-like behaviors.Additionally,specific knockdown of astrocytic S1P1 inhibited neuroinflammatory responses and attenuated blood-brain barrier leakage,seizure severity,and epilepsy-associated depression-like behaviors.Taken together,our results suggest that astrocytic sphingosine 1-phosphate receptor 1 exacerbates blood-brain barrier disruption in the epileptic brain by promoting neuroinflammation.

关键词： adeno-associated virus astrocytes blood-brain barrier epilepsy epilepsy-associated depression-like behavior neuroinflammation pentylenetetrazol pilocarpine tight junction

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Overexpression of ACE2 ameliorates Aβ-induced blood–brain barrier damage and angiogenesis by inhibiting NF-κB/VEGF/VEGFR2 pathway

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Animal Models and Experimental Medicine 2023年第3期6卷 237-244页

作者： Xueling Zhang Yu Zhang Ling Zhang Chuan Qin Institute of Laboratory Animal Sciences CAMS&PUMCBeijingChina National Human Diseases Animal Model Resource Center BeijingChina NHC Key Laboratory of Human Disease Comparative Medicine BeijingChina Changping National Laboratory(CPNL) BeijingChina

Background:Pathological angiogenesis and blood–brain barrier damage may play an important role in Alzheimer's disease(AD).ACE2 is mainly expressed on the surface of endothelial cells in brain.Recent studies have shown that the expression of ACE2 in AD is reduced,but its role in AD is still unclear.Method:We induced AD damage in endothelial cells using Aβ25-35 and overexpressed ACE2 in bEend.3 cells through lentiviral transfection.We detected the effect of Aβ25-35 on cell viability using the CCK-8 assay and examined the effect of overexpressing ACE2 on angiogenesis using an angiogenesis assay.We used western blot and cell immunofluorescence to detect changes in the expression of the VEGF/VEGFR2 pathway,tight junction protein,and NF-κB pathway.Results:Aβ25-35 treatment significantly decreased the expression of ACE2 and reduced cell viability.ACE2 overexpression(1)reduced the number of branches and junctions in tube formation,(2)inhibited the activation of the VEGF/VEGFR2 pathway induced by Aβ25-35,(3)increased the expression of TJPs,including ZO-1 and claudin-5,and(4)restored Aβ25-35-induced activation of the NF-κB pathway.Conclusion:Overexpression of ACE2 can improve pathological angiogenesis and blood–brain barrier damage in AD models in vitro by inhibiting NF-κB/VEGF/VEGFR2 pathway activity.ACE2 may therefore represent a therapeutic target for endothelial cell dysfunction in AD.

关键词： ACE2 Alzheimer's disease angiogenesis blood-brain barrier VEGF

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