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Neural stem cell-derived exosomes regulate cell proliferation,migration,and cell death of brain microvascular endothelial cells via the miR-9/Hes1 axis under hypoxia
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作者 Xiaojun Deng Xiaoyi Hu +8 位作者 Shang Wang Hui Zhao Yaqin Wei Jiaqi Fu Wenhui Wu Jinming Liu Caicai Zhang Lili Wang Ping Yuan 《Animal Models and Experimental Medicine》 CAS CSCD 2024年第1期24-35,共12页
Background:Our previous study found that mouse embryonic neural stem cell(NSC)-derived exosomes(EXOs)regulated NSC differentiation via the miR-9/Hes1 axis.However,the effects of EXOs on brain microvascular endothelial... Background:Our previous study found that mouse embryonic neural stem cell(NSC)-derived exosomes(EXOs)regulated NSC differentiation via the miR-9/Hes1 axis.However,the effects of EXOs on brain microvascular endothelial cell(BMEC)dysfunction via the miR-9/Hes1 axis remain unknown.Therefore,the current study aimed to determine the effects of EXOs on BMEC proliferation,migration,and death via the miR-9/Hes1 axis.Methods:Immunofluorescence,quantitative real-time polymerase chain reaction,cell counting kit-8 assay,wound healing assay,calcein-acetoxymethyl/propidium iodide staining,and hematoxylin and eosin staining were used to determine the role and mechanism of EXOs on BMECs.Results:EXOs promoted BMEC proliferation and migration and reduced cell death under hypoxic conditions.The overexpression of miR-9 promoted BMEC prolifera-tion and migration and reduced cell death under hypoxic conditions.Moreover,miR-9 downregulation inhibited BMEC proliferation and migration and also promoted cell death.Hes1 silencing ameliorated the effect of amtagomiR-9 on BMEC proliferation and migration and cell death.Hyperemic structures were observed in the regions of the hippocampus and cortex in hypoxia-induced mice.Meanwhile,EXO treatment improved cerebrovascular alterations.Conclusion:NSC-derived EXOs can promote BMEC proliferation and migra-tion and reduce cell death via the miR-9/Hes1 axis under hypoxic conditions.Therefore,EXO therapeutic strategies could be considered for hypoxia-induced vascular injury. 展开更多
关键词 brain microvascular endothelial cells EXOSOMES HES1 MIR-9 neural stem cells
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Crosstalk among Oxidative Stress,Autophagy,and Apoptosis in the Protective Effects of Ginsenoside Rb1 on Brain Microvascular Endothelial Cells:A Mixed Computational and Experimental Study
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作者 Yi-miao LUO Shu-sen LIU +5 位作者 Ming ZHAO Wei WEI Jiu-xiu YAO Jia-hui SUN Yu CAO Hao LI 《Current Medical Science》 SCIE CAS 2024年第3期578-588,共11页
Objective Brain microvascular endothelial cells (BMECs) were found to shift from their usually inactive state to an active state in ischemic stroke (IS) and cause neuronal damage. Ginsenoside Rb1 (GRb1),a component de... Objective Brain microvascular endothelial cells (BMECs) were found to shift from their usually inactive state to an active state in ischemic stroke (IS) and cause neuronal damage. Ginsenoside Rb1 (GRb1),a component derived from medicinal plants,is known for its pharmacological benefits in IS,but its protective effects on BMECs have yet to be explored. This study aimed to investigate the potential protective effects of GRb1 on BMECs. Methods An in vitro oxygen-glucose deprivation/reperfusion (OGD/R) model was established to mimic ischemia-reperfusion (I/R) injury. Bulk RNA-sequencing data were analyzed by using the Human Autophagy Database and various bioinformatic tools,including gene set enrichment analysis (GSEA),Gene Ontology (GO) classification and enrichment analysis,Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis,protein-protein interaction network analysis,and molecular docking. Experimental validation was also performed to ensure the reliability of our findings. Results Rb1 had a protective effect on BMECs subjected to OGD/R injury. Specifically,GRb1 was found to modulate the interplay between oxidative stress,apoptosis,and autophagy in BMECs. Key targets such as sequestosome 1 (SQSTM1/p62),autophagy related 5 (ATG5),and hypoxia-inducible factor 1-alpha (HIF-1α) were identified,highlighting their potential roles in mediating the protective effects of GRb1 against IS-induced damage. Conclusion GRbl protects BMECs against OGD/R injury by influencing oxidative stress,apoptosis,and autophagy. The identification of SQSTM1/p62,ATG5,and HIF-1α as promising targets further supports the potential of GRb1 as a therapeutic agent for IS,providing a foundation for future research into its mechanisms and applications in IS treatment. 展开更多
关键词 ischemic stroke ginsenoside Rb1 brain microvascular endothelial cells oxidative stress AUTOPHAGY APOPTOSIS bioinformatic analysis
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β-Estradiol 17-acetate enhances the in vitro vitality of endothelial cells isolated from the brain of patients subjected to neurosurgery 被引量:1
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作者 Sonia Guzzo Pasquale De Bonis +1 位作者 Barbara Pavan Luciano Fadiga 《Neural Regeneration Research》 SCIE CAS CSCD 2023年第2期389-395,共7页
In the current landscape of endothelial cell isolation for building in vitro models of the blood-brain barrier,our work moves towards reproducing the features of the neurovascular unit to achieve glial compliance thro... In the current landscape of endothelial cell isolation for building in vitro models of the blood-brain barrier,our work moves towards reproducing the features of the neurovascular unit to achieve glial compliance through an innovative biomimetic coating technology for brain chronic implants.We hypothesized that the autologous origin of human brain mic rovascular endothelial cells(hBMECs)is the first requirement for the suitable coating to prevent the glial inflammato ry response trigge red by foreign neuroprosthetics.Therefo re,this study established a new procedure to preserve the in vitro viability of hBMECs isolated from gray and white matter specimens taken from neurosurge ry patients.Culturing adult hBMECs is generally considered a challenging task due to the difficult survival ex vivo and progressive reduction in proliferation of these cells.The addition of 10 nMβ-estradiol 17-acetate to the hBMEC culture medium was found to be an essential and discriminating factor promoting adhesion and proliferation both after isolation and thawing,suppo rting the well-known protective role played by estrogens on microvessels.In particular,β-estradiol 17-acetate was critical for both freshly isolated and thawed female-derived hBMECs,while it was not necessary for freshly isolated male-derived hBMECs;however,it did countera ct the decay in the viability of the latter after thawing.The tumo r-free hBMECs were thus cultured for up to 2 months and their growth efficiency was assessed befo re and after two periods of cryopreservation.Des pite the thermal stress,the hBMECs remained viable and suitable for re-freezing and storage for several months.This approach increasing in vitro viability of hBMECs opens new perspectives for the use of cryopreserved autologous hBMECs as biomimetic therapeutic tools,offering the potential to avoid additional surgical sampling for each patient. 展开更多
关键词 β-estradiol 17-acetate 17Β-ESTRADIOL CRYOPRESERVATION GENDER-SPECIFIC gray matter human brain microvascular endothelial cells surgical resections vascular protection white matter
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Targeting brain microvascular endothelial cells: a therapeutic approach to neuroprotection against stroke 被引量:22
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作者 Qi-jin Yu Hong Tao +1 位作者 Xin Wang Ming-chang Li 《Neural Regeneration Research》 SCIE CAS CSCD 2015年第11期1882-1891,共10页
Brain microvascular endothelial cells form the interface between nervous tissue and circulating blood, and regulate central nervous system homeostasis. Brain microvascular endothelial cells differ from peripheral endo... Brain microvascular endothelial cells form the interface between nervous tissue and circulating blood, and regulate central nervous system homeostasis. Brain microvascular endothelial cells differ from peripheral endothelial cells with regards expression of specific ion transporters and receptors, and contain fewer fenestrations and pinocytotic vesicles. Brain microvascular endothelial cells also synthesize several factors that influence blood vessel function. This review describes the morphological characteristics and functions of brain microvascular endothelial cells, and summarizes current knowledge regarding changes in brain microvascular endothelial cells during stroke progression and therapies. Future studies should focus on identifying mechanisms underlying such changes and developing possible neuroprotective therapeutic interventions. 展开更多
关键词 nerve regeneration blood-brain barrier brain microvascular endothelial cells cerebralinfarction subarachnoid hemorrhage gap junction ENDOTHELIN thromboxane A2 neural regeneration
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In vitro model of the blood-brain barrier established by co-culture of primary cerebral microvascular endothelial and astrocyte cells 被引量:7
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作者 Yan Wang Ning Wang +3 位作者 Biao Cai Guang-yun Wang Jing Li Xing-xing Piao 《Neural Regeneration Research》 SCIE CAS CSCD 2015年第12期2011-2017,共7页
Drugs for the treatment and prevention of nervous system diseases must permeate the bloodbrain barrier to take effect.In vitro models of the blood-brain barrier are therefore important in the investigation of drug per... Drugs for the treatment and prevention of nervous system diseases must permeate the bloodbrain barrier to take effect.In vitro models of the blood-brain barrier are therefore important in the investigation of drug permeation mechanisms.However,to date,no unified method has been described for establishing a blood-brain barrier model.Here,we modified an in vitro model of the blood-brain barrier by seeding brain microvascular endothelial cells and astrocytes from newborn rats on a polyester Transwell cell culture membrane with 0.4-μm pores,and conducted transepithelial electrical resistance measurements,leakage tests and assays for specific bloodbrain barrier enzymes.We show that the permeability of our model is as low as that of the bloodbrain barrier in vivo.Our model will be a valuable tool in the study of the mechanisms of action of neuroprotective drugs. 展开更多
关键词 nerve regeneration blood-brain barrier ASTROCYTES brain microvascular endothelial cells permeability CO-CULTURE Transwell chamber neural regeneration
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Hypoxia inducible factor-1alpha mediates protection of DL-3-n-butylphthalide in brain microvascular endothelial cells against oxygen glucose deprivation-induced injury 被引量:7
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作者 Weihong Yang Ling Li +3 位作者 Ruxun Huang Zhong Pei Songjie Liao Jinsheng Zeng 《Neural Regeneration Research》 SCIE CAS CSCD 2012年第12期948-954,共7页
Studies have demonstrated that DL-3-n-butylphthalide can significantly alleviate oxygen glucose deprivation-induced injury of human umbilical vein endothelial cells at least partly associated with its enhancement on o... Studies have demonstrated that DL-3-n-butylphthalide can significantly alleviate oxygen glucose deprivation-induced injury of human umbilical vein endothelial cells at least partly associated with its enhancement on oxygen glucose deprivation-induced hypoxia inducible factor-1α expression.In this study,we hypothesized that DL-3-n-butylphthalide can protect against oxygen glucose deprivation-induced injury of newborn rat brain microvascular endothelial cells by means of upregulating hypoxia inducible factor-1α expression.MTT assay and Hoechst staining results showed that DL-3-n-butylphthalide protected brain microvascular endothelial cells against oxygen glucose deprivation-induced injury in a dose-dependent manner.Western blot and immunofluorescent staining results further confirmed that the protective effect was related to upregulation of hypoxia inducible factor-1α.Real-time RT-PCR reaction results showed that DL-3-n-butylphthalide reduced apoptosis by inhibiting downregulation of pro-apoptotic gene caspase-3 mRNA expression and upregulation of apoptosis-executive protease bcl-2 mRNA expression;however,DL-3-n-butylphthalide had no protective effects on brain microvascular endothelial cells after knockdown of hypoxia inducible factor-1α by small interfering RNA.These findings suggest that DL-3-n-butylphthalide can protect brain microvascular endothelial cells against oxygen glucose deprivation-induced injury by upregulating bcl-2 expression and downregulating caspase-3 expression though hypoxia inducible factor-1α pathway. 展开更多
关键词 DL-3-n-butylphthalide APOPTOSIS brain microvascular endothelial cells hypoxia inducible factor-1α
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Polylactic Acid Nanoparticles Targeted to Brain Microvascular Endothelial Cells 被引量:1
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作者 王华芳 胡豫 +1 位作者 孙望强 谢长生 《Journal of Huazhong University of Science and Technology(Medical Sciences)》 SCIE CAS 2005年第6期642-644,共3页
In this work, blank polylactic acid (PLA) nanoparticles with unstained surface were prepared by the nano-deposition method. On the basis of the preparation, the effect of surface modification on brain microvascular ... In this work, blank polylactic acid (PLA) nanoparticles with unstained surface were prepared by the nano-deposition method. On the basis of the preparation, the effect of surface modification on brain microvascular endothelial cells (BMECs) targeting was examined by in vivo experiments and fluorescence microscopy. The results showed that PLA nanoparticles are less toxic than PACA nanoparticles but their BMECs targeting is similar to PACA nanoparticles. The experiments suggest that drugs can he loaded onto the particles and become more stable through adsorption on the surface of PLA nanoparticles with high surface activity. The surface of PLA nanoparticles was obviously modified and the hydrophilicity was increased as well in the presence of non-ionic surfactants on PLA nanoparticles. As a targeting moiety, polysobate 80 (T-80) can facilitate BMECs targeting of PLA nanoparticles. 展开更多
关键词 polylactic acid nanoparticles polysorbate brain microvascular endothelial cells TARGETING
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Protective effect of Cordyceps sinensis extract on rat brain microvascular endothelial cells injured by oxygen-glucose deprivation 被引量:1
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作者 Xue Bai Yibo Tang +7 位作者 Yan Lin Yuqing Zhao Tianyang Tan Shuyan Wang Meiqi Liu Zhenghui Chang Ying Liu Zhenquan Liu 《Journal of Traditional Chinese Medical Sciences》 2018年第1期64-71,共8页
Objective:To investigate the protective effect of Cordyceps sinensis extract (CSE)on injury of primary cultured rat brain microvascular endothelial cells (rBMECs) induced by oxygen-glucose deprivation (OGD).Methods:We... Objective:To investigate the protective effect of Cordyceps sinensis extract (CSE)on injury of primary cultured rat brain microvascular endothelial cells (rBMECs) induced by oxygen-glucose deprivation (OGD).Methods:We isolated and cultured primary rBMECs in order to establish an in vitro OGD model.Cellular activity was detected using a cell counting kit to determine the appropriate dosage.The rBMECs were divided into control,model,low-,mid-,and high-dose (5,10,20 μg.mL-1) CSE groups under OGD for 6 hours.CSE was dissolved in cell culture medium to the appropriate concentration,passed through a 0.22 μm sterile filter,and administered for 12 hours before and during OGD.Cellular morphology was observed under a microscope.Lactate dehydrogenase level in cultural supernatant,superoxide dismutase activity,and the content of nitric oxide and malondialdehyde in cells were tested by colorimetric methods.Levels of tumor necrosis factor-α and interleukin-1 beta in cells were determined by enzyme-linked immunosorbent assay.Results:After 12-hour administration of CSE at the concentration of 5,10,20 iμg.mL-1 before and during OGD,compared with the model group,the CSE groups obviously alleviated the damage of rBMECs induced by OGD,inhibited the apoptosis and the necrosis of the cells,and improved cellular morphology of rBMECs.Additionally,compared with the model group,CSE also restrained lactate dehydrogenase leakage in hypoxic cells (P <.01),significantly increased superoxide dismutase activity (P <.05),and reduced the levels of nitric oxide,malondialdehyde,tumor necrosis factor-α,and interleukin-1 beta (P <.05).Conclusion:C.sinensis extract plays a significant role in protecting injured primary cultured rBMECs induced by OGD.The mechanism may be related with the increase of cellular antioxidative capacity and anti-inflammatory effect. 展开更多
关键词 CORDYCEPS sinensis EXTRACT brain microvascular endothelial cells Oxygen-glucose DEPRIVATION ANTI-OXIDATION Anti-inflammation
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The role of heme-oxygenase-1 in pathogenesis of cerebral malaria in the co-culture model of human brain microvascular endothelial cell and ITG Plasmodium falciparum-infected red blood cells
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作者 Pimwan Thongdee Kesara Na-Bangchang 《Asian Pacific Journal of Tropical Medicine》 SCIE CAS 2017年第1期20-24,共5页
Objective: To investigate the role of human host heme-oxygenase-1(HO-1) in pathogenesis of cerebral malaria in the in vitro model,Methods: The effect of human host HO-1 [human brain microvascular endothelial cell(HBME... Objective: To investigate the role of human host heme-oxygenase-1(HO-1) in pathogenesis of cerebral malaria in the in vitro model,Methods: The effect of human host HO-1 [human brain microvascular endothelial cell(HBMEC)] on hemoglobin degradation in the co-culture model of HBMEC and ITG Plasmodium falciparum-infected red cells(i RBC) through measurement of the enzymatic products iron and bilirubin,Results: Following exposure to the HO-1 inducer Co PPIX at all concentrations,the HBMEC cells apoptosis occurred,which could be prominently observed at 15 μM of 3 h exposure,In contrast,there was no significant change in the morphology in the non-exposed i RBC at all concentrations and exposure time,This observation was in agreement with the levels of the enzymatic degradation products iron and bilirubin,of which the highest levels(106.03 and 1 753.54% of baseline level,respectively) were observed at 15 μM vs,20 μM at 3 h vs,24 h exposure,For the effect of the HO-1 inhibitor Zn PPIX,HBMEC cell morphology was mostly unchanged,but significant inhibitory effect on cell apoptosis was seen at 10 μM for the exposure period of 3 h(37.17% of baseline level),The degree of the inhibitory effect as reflected by the level of iron produced was not clearly observed(highest effect at 10 μM and 3 h exposure),Conclusions: Results provide at least in part,insight into the contribution of HO-1 on CM pathogenesis and need to be confirmed in animal model. 展开更多
关键词 Plasmodium falciparum Heme-oxygenase-1 Zn(Ⅱ)-protoporphyrin inhibitor Co-protoporphyrin inducer Human brain microvascular endothelial cell
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Primary culture and identification about brain microvascular endothelial cells of rabbits
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作者 MA Hua-gen LIU Zhao-de +1 位作者 LIU Hai-qin TANG Yuan-yu 《Journal of Hainan Medical University》 2022年第19期6-10,共5页
Objective:To establish a simple and efficient culture method of primary rabbit brain microvascular endothelial cells,provide important carriers and tool cells for the research of related cerebrovascular diseases.Metho... Objective:To establish a simple and efficient culture method of primary rabbit brain microvascular endothelial cells,provide important carriers and tool cells for the research of related cerebrovascular diseases.Methods:The cerebral cortexes of rabbits were collected aseptic and inoculated after cutting,passing through cell sieve,bovine serum albumin density gradient centrifugation,typeⅡcollagenase digestion,finally inoculated and cultured.The cultured cells were identified by cell morphological observation and angiogenesis experiment.Results:Under the inverted microscope,the cells were short fusiform or polygonal,and grew in clusters and adhere to the wall.After the cells were densely fused,they would be in a typical monolayer flat,“pebbled"mosaic arrangement.Tube formation test had the ability to form tubes structure.Conclusion:This method can successfully separate and cultivate primary rabbit brain microvascular endothelial cells. 展开更多
关键词 RABBIT brain microvascular endothelial cells Primary culture Morphologic observation Tube formation test
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Sustained release of vascular endothelial growth factor A and basic fibroblast growth factor from nanofiber membranes reduces oxygen/glucose deprivation-induced injury to neurovascular units 被引量:3
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作者 Yifang Wu Jun Sun +2 位作者 Qi Lin Dapeng Wang Jian Hai 《Neural Regeneration Research》 SCIE CAS CSCD 2024年第4期887-894,共8页
Upregulation of vascular endothelial growth factor A/basic fibroblast growth factor(VEGFA/b FGF)expression in the penumbra of cerebral ischemia can increase vascular volume,reduce lesion volume,and enhance neural cell... Upregulation of vascular endothelial growth factor A/basic fibroblast growth factor(VEGFA/b FGF)expression in the penumbra of cerebral ischemia can increase vascular volume,reduce lesion volume,and enhance neural cell proliferation and differentiation,thereby exerting neuroprotective effects.However,the beneficial effects of endogenous VEGFA/b FGF are limited as their expression is only transiently increased.In this study,we generated multilayered nanofiber membranes loaded with VEGFA/b FGF using layer-by-layer self-assembly and electrospinning techniques.We found that a membrane containing 10 layers had an ideal ultrastructure and could efficiently and stably release growth factors for more than 1 month.This 10-layered nanofiber membrane promoted brain microvascular endothelial cell tube formation and proliferation,inhibited neuronal apoptosis,upregulated the expression of tight junction proteins,and improved the viability of various cellular components of neurovascular units under conditions of oxygen/glucose deprivation.Furthermore,this nanofiber membrane decreased the expression of Janus kinase-2/signal transducer and activator of transcription-3(JAK2/STAT3),Bax/Bcl-2,and cleaved caspase-3.Therefore,this nanofiber membrane exhibits a neuroprotective effect on oxygen/glucose-deprived neurovascular units by inhibiting the JAK2/STAT3 pathway. 展开更多
关键词 brain ischemia brain microvascular endothelial cell nanofiber membrane neurovascular unit
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Shuxuetong injection protects cerebral microvascular endothelial cells against oxygen-glucose deprivation reperfusion 被引量:14
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作者 Zuo-Yan Sun Fu-Jiang Wang +6 位作者 Hong Guo Lu Chen Li-Juan Chai Rui-Lin Li Li-Min Hu Hong Wang Shao-Xia Wang 《Neural Regeneration Research》 SCIE CAS CSCD 2019年第5期783-793,共11页
Shuxuetong injection composed of leech(Hirudo nipponica Whitman) and earthworm(Pheretima aspergillum) has been used for the clinical treatment of acute stroke for many years in China. However, the precise neuroprotect... Shuxuetong injection composed of leech(Hirudo nipponica Whitman) and earthworm(Pheretima aspergillum) has been used for the clinical treatment of acute stroke for many years in China. However, the precise neuroprotective mechanism of Shuxuetong injection remains poorly understood. Here, cerebral microvascular endothelial cells(bEnd.3) were incubated in glucose-free Dulbecco's modified Eagle's medium containing 95% N_2/5% CO_2 for 6 hours, followed by high-glucose medium containing 95% O_2 and 5% CO_2 for 18 hours to establish an oxygen-glucose deprivation/reperfusion model. This in vitro cell model was administered Shuxuetong injection at 1/32, 1/64, and 1/128 concentrations(diluted 32-, 64-, and 128-times). Cell Counting Kit-8 assay was used to evaluate cell viability. A fluorescence method was used to measure lactate dehydrogenase, and a fluorescence microplate reader used to detect intracellular reactive oxygen species. A fluorescent probe was also used to measure mitochondrial superoxide production. A cell resistance meter was used to measure transepithelial resistance and examine integrity of monolayer cells. The fluorescein isothiocyanate-dextran test was performed to examine blood-brain barrier permeability. Real-time reverse transcription polymerase chain reaction was performed to analyze mRNA expression levels of tumor necrosis factor alpha, interleukin-1β, interleukin-6, and inducible nitric oxide synthase. Western blot assay was performed to analyze expression of caspase-3, intercellular adhesion molecule 1, vascular cell adhesion molecule 1, occludin, vascular endothelial growth factor, cleaved caspase-3, B-cell lymphoma 2, phosphorylated extracellular signal-regulated protein kinase, extracellular signal-regulated protein kinase, nuclear factor-κB p65, I kappa B alpha, phosphorylated I kappa B alpha, I kappa B kinase, phosphorylated I kappa B kinase, claudin-5, and zonula occludens-1. Our results show that Shuxuetong injection increases bEnd.3 cell viability and B-cell lymphoma 2 expression, reduces cleaved caspase-3 expression, inhibits production of reactive oxygen species and mitochondrial superoxide, suppresses expression of tumor necrosis factor alpha, interleukin-1β, interleukin-6, inducible nitric oxide synthase mRNA, intercellular adhesion molecule-1, and vascular cell adhesion molecule-1, markedly increases transepithelial resistance, decreases blood-brain barrier permeability, upregulates claudin-5, occludin, and zonula occludens-1 expression, reduces nuclear factor-κB p65 and vascular endothelial growth factor expression, and reduces I kappa B alpha, extracellular signal-regulated protein kinase 1/2, and I kappa B kinase phosphorylation levels. Overall, these findings suggest that Shuxuetong injection has protective effects on brain microvascular endothelial cells after oxygen-glucose deprivation/reperfusion. Moreover, its protective effect is associated with reduction of mitochondrial superoxide production, inhibition of the inflammatory response, and inhibition of vascular endothelial growth factor, extracellular signal-regulated protein kinase 1/2, and the nuclear factor-κB p65 signaling pathway. 展开更多
关键词 nerve REGENERATION SHUXUETONG injection brain microvascular endothelial cells oxygen-glucose deprivation/reperfusion tight junction proteins mitochondrial function inflammatory factors blood-brain barrier neuroprotection neural REGENERATION
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LncRNA SNHG12 ameliorates brain microvascular endothelial cell injury by targeting miR-199a 被引量:21
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作者 Fa-Qing Long Qing-Jie Su +4 位作者 Jing-Xia Zhou De-Sheng Wang Peng-Xiang Li Chao-Sheng Zeng, Yi Cai 《Neural Regeneration Research》 SCIE CAS CSCD 2018年第11期1919-1926,共8页
Long non-coding RNAs regulate brain microvascular endothelial cell death, the inflammatory response and angiogenesis during and after ischemia/reperfusion and oxygen-glucose deprivation/reoxygenation(OGD/R) insults.... Long non-coding RNAs regulate brain microvascular endothelial cell death, the inflammatory response and angiogenesis during and after ischemia/reperfusion and oxygen-glucose deprivation/reoxygenation(OGD/R) insults. The long non-coding RNA, SNHG12, is upregulated after ischemia/reperfusion and OGD/R in microvascular endothelial cells of the mouse brain. However, its role in ischemic stroke has not been studied. We hypothesized that SNHG12 positively regulates ischemic stroke, and therefore we investigated its mechanism of action. We established an OGD/R mouse cell model to mimic ischemic stroke by exposing brain microvascular endothelial cells to OGD for 0, 2, 4, 8, 16 or 24 hours and reoxygenation for 4 hours. Quantitative real-time polymerase chain reaction showed that SNHG12 levels in brain microvascular endothelial cells increased with respect to OGD exposure time. Brain microvascular endothelial cells were transfected with pc DNA-control, pc DNA-SNHG12, si-control, or si-SNHG12. After exposure to OGD for 16 hours, these cells were then analyzed by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide, trypan blue exclusion, western blot, and capillary-like tube formation assays. Overexpression of SNHG12 inhibited brain microvascular endothelial cell death and the inflammatory response but promoted angiogenesis after OGD/R, while SNHG12 knockdown had the opposite effects. miR-199a was identified as a target of SNHG12, and SNHG12 overexpression reversed the effect of miR-199a on brain microvascular endothelial cell death, the inflammatory response, and angiogenesis. These findings suggest that SNHG12 suppresses endothelial cell injury induced by OGD/R by targeting miR-199a. 展开更多
关键词 nerve regeneration ischemic stroke microRNA brain microvascular endothelial cell death inflammatory response ANGIOGENESIS oxygen-glucose deprivation/reoxygenation ISCHEMIA/REPERFUSION therapeutic targets neural regeneration gene regulation neural regeneration
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Post-acute ischemic stroke hyperglycemia aggravates destruction of the blood-brain barrier 被引量:1
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作者 Tianqi Xu Jianhong Yang +5 位作者 Yao Xu Xiaofeng Wang Xiang Gao Jie Sun Chenhui Zhou Yi Huang 《Neural Regeneration Research》 SCIE CAS CSCD 2024年第6期1344-1350,共7页
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 bloo... 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. 展开更多
关键词 acute ischemic stroke blood-brain barrier brain microvascular endothelial cells mitochondrial transfer stress hyperglycemia
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Integrin binding peptides facilitate growth and interconnected vascular-like network formation of rat primary cortical vascular endothelial cells in vitro
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作者 Ram Kuwar Xuejun Wen +1 位作者 Ning Zhang Dong Sun 《Neural Regeneration Research》 SCIE CAS CSCD 2023年第5期1052-1056,共5页
Neovascularization and angiogenesis in the brain are important physiological processes for normal brain development and repair/regeneration following insults. Integrins are cell surface adhesion receptors mediating im... Neovascularization and angiogenesis in the brain are important physiological processes for normal brain development and repair/regeneration following insults. Integrins are cell surface adhesion receptors mediating important function of cells such as survival, growth and development during tissue organization, differentiation and organogenesis. In this study, we used an integrin-binding array platform to identify the important types of integrins and their binding peptides that facilitate adhesion, growth, development, and vascular-like network formation of rat primary brain microvascular endothelial cells. Brain microvascular endothelial cells were isolated from rat brain on post-natal day 7. Cells were cultured in a custom-designed integrin array system containing short synthetic peptides binding to 16 types of integrins commonly expressed on cells in vertebrates. After 7 days of culture, the brain microvascular endothelial cells were processed for immunostaining with markers for endothelial cells including von Willibrand factor and platelet endothelial cell adhesion molecule. 5-Bromo-2′-dexoyuridine was added to the culture at 48 hours prior to fixation to assess cell proliferation. Among 16 integrins tested, we found that α5β1, αvβ5 and αvβ8 greatly promoted proliferation of endothelial cells in culture. To investigate the effect of integrin-binding peptides in promoting neovascularization and angiogenesis, the binding peptides to the above three types of integrins were immobilized to our custom-designed hydrogel in three-dimensional(3 D) culture of brain microvascular endothelial cells with the addition of vascular endothelial growth factor. Following a 7-day 3 D culture, the culture was fixed and processed for double labeling of phalloidin with von Willibrand factor or platelet endothelial cell adhesion molecule and assessed under confocal microscopy. In the 3 D culture in hydrogels conjugated with the integrin-binding peptide, brain microvascular endothelial cells formed interconnected vascular-like network with clearly discernable lumens, which is reminiscent of brain microvascular network in vivo. With the novel integrin-binding array system, we identified the specific types of integrins on brain microvascular endothelial cells that mediate cell adhesion and growth followed by functionalizing a 3 D hydrogel culture system using the binding peptides that specifically bind to the identified integrins, leading to robust growth and lumenized microvascular-like network formation of brain microvascular endothelial cells in 3 D culture. This technology can be used for in vitro and in vivo vascularization of transplants or brain lesions to promote brain tissue regeneration following neurological insults. 展开更多
关键词 3D culture angiogenesis brain microvascular endothelial cells hydrogel INTEGRINS platelet endothelial cell adhesion molecule(PECAM-1) vascular endothelial growth factor(VEGF) VASCULARIZATION
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常压高浓度氧对新生大鼠脑微血管内皮细胞损伤与Nrf2/HO-1信号通路的影响分析 被引量:1
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作者 张占伟 谭焱 +2 位作者 田桂湘 范瑶 王佳怡 《临床和实验医学杂志》 2024年第3期233-237,共5页
目的探究常压高浓度氧(NBO)对新生大鼠脑微血管内皮细胞损伤及核因子E2相关因子2/血红素氧合酶-1(Nrf2/HO-1)信号通路的影响。方法取新生SD大鼠45只,采用随机数字表法分为常氧组、NBO组和NBO+Nrf2激活剂组,每组各15只。常氧组大鼠置于... 目的探究常压高浓度氧(NBO)对新生大鼠脑微血管内皮细胞损伤及核因子E2相关因子2/血红素氧合酶-1(Nrf2/HO-1)信号通路的影响。方法取新生SD大鼠45只,采用随机数字表法分为常氧组、NBO组和NBO+Nrf2激活剂组,每组各15只。常氧组大鼠置于普通空气(21%氧气)中饲养,NBO组和NBO+Nrf2激活剂组大鼠置于90%常压氧气饲养,NBO+Nrf2激活剂组每日灌胃5 mg/kg Nrf2激动剂莱菔硫烷。测定脑组织伊文思蓝(EB)含量,采用酶联免疫法检测血管内皮生长因子(VEGF)和基质金属蛋白酶9(MMP-9)含量,干湿重法检测脑组织含水量,HE染色和TUNEL染色观察脑组织病理变化,蛋白质印迹法检测海马组织Nrf2/HO-1信号通路蛋白表达,水迷宫检测大鼠认知功能。结果与常氧组比较,NBO组脑组织EB、VEGF、MMP-9含量及脑组织含水量升高,差异均有统计学意义(P<0.05);与NBO组比较,NBO+Nrf2激活剂组脑组织EB、VEGF、MMP-9含量及脑组织含水量降低,差异均有统计学意义(P<0.05)。病理染色结果显示,常氧组大鼠神经细胞形态及结构完整,未见明显病理变化和细胞凋亡;NBO组神经细胞形态及结构不规则,出现明显的水肿和空泡,并伴有大量的凋亡细胞;NBO+Nrf2激活剂组脑组织病理损伤较NBO组明显减轻。与常氧组比较,NBO组脑组织Nrf2、HO-1蛋白相对表达量降低,差异均有统计学意义(P<0.05);与NBO组比较,NBO+Nrf2激活剂组Nrf2、HO-1蛋白相对表达量升高,差异均有统计学意义(P<0.05)。与常氧组比较,NBO组第2~4天逃避潜伏期延长,穿越平台次数减少,差异均有统计学意义(P<0.05);与NBO组比较,NBO+Nrf2激活剂组第2~4天逃避潜伏期缩短,穿越平台次数增多,差异均有统计学意义(P<0.05)。结论NBO可诱导新生大鼠脑微血管内皮细胞损伤,导致远期认知功能障碍,可能与下调Nrf2/HO-1信号通路表达有关。 展开更多
关键词 常压高浓度氧 新生大鼠 微血管内皮细胞损伤 血脑屏障功能 认知功能障碍 核因子E2相关因子2/血红素氧合酶-1信号通路
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基于IP联合蛋白质组学探讨ENG互作蛋白在bEnd.3细胞中的作用
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作者 陈清杰 李奥迪 +4 位作者 季慧敏 孙艺瑄 蒋越 叶子奇 潘荣 《湖北科技学院学报(医学版)》 2024年第6期461-466,F0002,共7页
目的本研究拟筛选并验证在脑微血管内皮细胞(bEnd.3)中Endoglin(ENG)的互作蛋白及其作用。方法采用蛋白质组学和生物信息学技术鉴定并富集ENG互作蛋白,对这些互作蛋白进行亚细胞定位、GO功能注释、IPR注释和蛋白互作网络等分析。将以上... 目的本研究拟筛选并验证在脑微血管内皮细胞(bEnd.3)中Endoglin(ENG)的互作蛋白及其作用。方法采用蛋白质组学和生物信息学技术鉴定并富集ENG互作蛋白,对这些互作蛋白进行亚细胞定位、GO功能注释、IPR注释和蛋白互作网络等分析。将以上分析筛选出的ENG互作蛋白,采用免疫共沉淀(IP)实验、细胞免疫荧光(IF)和蛋白免疫印迹(WB)技术进行验证和对比,探究ENG互作蛋白在棕榈酸(PA)、基因沉默和过表达ENG处理bEnd.3细胞中的表达变化及作用。结果通过蛋白质组学分析,bEnd.3细胞中ENG互作蛋白在亚细胞定位分析中细胞骨架相关成分呈现出较高的占比;通过GO注释和IPR注释进一步发现,是细胞骨架中的中间纤维和微丝蛋白呈现较高的富集状态。ENG与细胞骨架蛋白互作热力图结果显示,与对照组相比,PA处理的bEnd.3细胞中微丝蛋白Filamin B(Flnb)数值显著降低。IP和IF结果显示,bEnd.3细胞中ENG与Flnb存在蛋白互作和共定位情况。WB结果显示,bEnd.3细胞在PA处理条件下,ENG和Flnb蛋白表达均下降;在ENG沉默条件下,Flnb蛋白随ENG表达的减少而降低;在ENG过表达条件下,Flnb蛋白随ENG表达的增加而升高。结论ENG互作蛋白广泛参与到多种相关的生物途径以及信号通路之中,ENG在bEnd.3细胞中与Flnb蛋白存在相互作用且二者具有共定位现象,ENG还能够调控PA处理的bEnd.3细胞Flnb蛋白表达水平。 展开更多
关键词 ENG Flnb 互作蛋白 bEnd.3 棕榈酸
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天麻素与薯蓣皂苷元配伍对大鼠缺氧损伤脑微血管内皮细胞的保护作用 被引量:1
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作者 王志昊 祝娜 +5 位作者 唐茂红 付饶 阿热依·巴哈提 李彦文 黄秀兰 李志勇 《医药导报》 CAS 北大核心 2024年第5期667-679,共13页
目的探讨天麻素(Gas)、薯蓣皂苷元(Dio)及其组合物(GDC)对大鼠缺氧损伤脑微血管内皮细胞(BMECs)的保护作用和对脑微血管新生的影响及其作用机制。方法将BMECs分为5组:正常对照组,模型对照组,Gas组(1、2、4、8、16、32μmol·L^(-1))... 目的探讨天麻素(Gas)、薯蓣皂苷元(Dio)及其组合物(GDC)对大鼠缺氧损伤脑微血管内皮细胞(BMECs)的保护作用和对脑微血管新生的影响及其作用机制。方法将BMECs分为5组:正常对照组,模型对照组,Gas组(1、2、4、8、16、32μmol·L^(-1)),Dio组(0.25、0.5、1、2、4、8μmol·L^(-1)),GDC组(Gas和Dio浓度分别为1和0.25、2和0.5、4和1、8和2、16和4、32和8μmol·L^(-1))。分组给药12 h后,对模型对照组、Gas组、Dio组和GDC组通过氧糖剥夺法建立BMECs缺氧模型。检测乳酸脱氢酶(LDH)漏出率、白细胞介素1β(IL-1β)含量、超氧化物歧化酶(SOD)活力、丙二醛(MDA)浓度;观察Hoechst 33258、FITC-Annexin V/PI染色,采用Transwell小室实验、细胞划痕实验和小管形成实验,考察Gas、Dio及GDC对缺氧损伤BMECs的保护作用及促进血管新生作用。进一步利用网络药理学和分子对接方法研究GDC抗脑缺血的作用机制。结果Gas、Dio以2、0.5μmol·L^(-1)组合时,可显著提高缺氧损伤BMECs细胞活力(P<0.05),促进细胞增殖;与模型对照组比较,Gas组LDH漏出率降低(P<0.05);Gas组、Dio组与GDC组IL-1β含量均显著下降(均P<0.05),Gas组、GDC组SOD活力升高(P<0.05),Gas组、Dio组以及GDC组凋亡小体减少。GDC可促进BMECs缺氧模型的增殖、侵袭、迁移以及小管形成,表明其在细胞水平上一定程度促进血管新生。网络药理学研究发现,Gas与半胱天冬酶3(CASP3)、过氧化物酶体增生激活受体γ(PPARG)、凝血因子Ⅱ(F2)、基质金属蛋白酶-9(MMP-9)、丝氨酸苏氨酸蛋白激酶(Akt)1蛋白具有良好的结合活性,Dio与内皮一氧化氮合成酶(NOS3)、KDR蛋白具有良好的结合活性,Gas、Dio可能主要通过血管内皮生长因子(VEGF)信号通路、丝裂原活化蛋白激酶(MAPK)信号通路、磷酯酰肌醇3-激酶(PI3K)-Akt信号通路以及缺氧诱导因子-1(HIF-1)信号通路调控脑缺血后血管新生。结论Gas、Dio及GDC具有抗缺氧损伤作用并可促进缺氧损伤后血管新生,作用机制可能与其作用于Akt1、NOS3、VEGFR2等蛋白,调控VEGF/Akt/MAPK等信号通路促进血管新生有关。 展开更多
关键词 天麻素 薯蓣皂苷元 脑缺血 脑微血管内皮细胞 血管新生
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六味地黄丸介导RAGE抑制MMP-2/MMP-9对Aβ_(1-40)损伤bEnd.3细胞紧密连接蛋白的影响
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作者 丁蕊 袁永 +3 位作者 贾亚泉 高爱社 张振强 宋军营 《中成药》 CAS CSCD 北大核心 2024年第2期424-430,共7页
目的探讨六味地黄丸对β淀粉样蛋白1-40(Aβ_(1-40))损伤的小鼠脑微血管内皮细胞(bEnd.3)的保护作用及其机制。方法采用CCK8法检测Aβ_(1-40)和六味地黄丸含药血清(MSLDP)对细胞活性的影响,筛选合适的作用浓度。将bEnd.3细胞分为对照组... 目的探讨六味地黄丸对β淀粉样蛋白1-40(Aβ_(1-40))损伤的小鼠脑微血管内皮细胞(bEnd.3)的保护作用及其机制。方法采用CCK8法检测Aβ_(1-40)和六味地黄丸含药血清(MSLDP)对细胞活性的影响,筛选合适的作用浓度。将bEnd.3细胞分为对照组、Aβ_(1-40)组、MSLDP+Aβ_(1-40)组和MSLDP组,采用Western blot检测低密度脂蛋白相关蛋白1(LRP1)、晚期糖基化终末产物受体(RAGE)、基质金属蛋白酶2(MMP-2)、MMP-9、闭锁小带蛋白-1(ZO-1)、脑源性神经营养因子(BDNF)蛋白表达,免疫荧光检测LRP1、RAGE、ZO-1表达;再将bEnd.3细胞分为对照组、Aβ_(1-40)组、FPS-ZM1(RAGE抑制剂)+Aβ_(1-40)组和FPS-ZM1+Aβ_(1-40)+MSLDP组,Western blot检测RAGE、MMP-9、MMP-2、ZO-1蛋白表达。结果Aβ_(1-40)呈剂量依赖性降低bEnd.3细胞活性(P<0.01),MSLDP对Aβ_(1-40)损伤的细胞活性具有保护作用(P<0.05,P<0.01),因此选择10μmol/L Aβ_(1-40)和10%MSLDP进行后续实验。与对照组比较,Aβ_(1-40)组RAGE、MMP-2、MMP-9蛋白表达升高(P<0.01),LRP1、ZO-1、BDNF蛋白表达降低(P<0.05,P<0.01),并且LRP1、ZO-1荧光强度降低(P<0.01),RAGE荧光增强(P<0.01);与Aβ_(1-40)组比较,MSLDP组RAGE、MMP-2、MMP-9蛋白表达和RAGE荧光强度降低(P<0.05,P<0.01),而LRP1、ZO-1、BDNF蛋白表达和LRP1、ZO-1荧光强度升高(P<0.05,P<0.01)。与Aβ_(1-40)组比较,Aβ_(1-40)+FPS-ZM1组MMP-2、MMP9、RAGE蛋白表达降低(P<0.05,P<0.01),ZO-1蛋白表达升高(P<0.05);Aβ_(1-40)+FPS-ZM1+MSLDP组MMP-2、MMP9、RAGE蛋白表达降低(P<0.01),ZO-1蛋白表达升高(P<0.01),FPS-ZM1和MSLDP联合使用的效果更佳。结论六味地黄丸能够保护Aβ_(1-40)损伤的脑微血管内皮的细胞紧密连接,减轻血脑屏障障碍,保护神经血管单元防治阿尔茨海默病,可能通过调节RAGE途径抑制MMP-2/MMP-9途径实现。 展开更多
关键词 六味地黄丸 阿尔茨海默病 脑微血管内皮细胞 β淀粉样蛋白1-40(Aβ_(1-40)) 晚期糖基化终末产物受体(RAGE) 基质金属蛋白酶家族(MMPs)
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血脑屏障结构与功能及缺血性中风损伤机制的研究进展
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作者 谭娇(综述) 苏湲淇 +1 位作者 徐晓玉 薛强(审校) 《现代医药卫生》 2024年第16期2820-2825,共6页
中风是世界范围内发病率、致残率、致死率均高的疾病。血脑屏障(BBB)是维持脑内微环境稳定的重要功能性结构,在中风初期即被破坏,是中风主要并发症,且会加重中风对脑组织的损害。同时,BBB结构与功能的完整性程度是预测中风后溶栓治疗和... 中风是世界范围内发病率、致残率、致死率均高的疾病。血脑屏障(BBB)是维持脑内微环境稳定的重要功能性结构,在中风初期即被破坏,是中风主要并发症,且会加重中风对脑组织的损害。同时,BBB结构与功能的完整性程度是预测中风后溶栓治疗和血栓切除术后出血转化风险的关键因素,也是预防急性中风进一步脑损伤的重要治疗靶点。该文将近年来关于BBB结构、功能、缺血性损伤变化,以及潜在治疗靶点的相关研究进行了综述,为进一步认识和理解缺血性中风BBB变化及保护性药物开发提供思路。 展开更多
关键词 缺血性中风 血脑屏障 脑微血管内皮细胞 紧密连接 神经炎症 综述
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