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1.
研究肾脏缺血再灌注( ischemia-reperfusion, IR)对小鼠肾脏血管内皮生长因子受体3( vascular endothelial growth factor receptor 3, VEGFR3)表达的影响。方法30只雄性C57BL/6小鼠随即分为5组:假手术组( Sham组)﹑缺血再灌注0﹑6、12﹑24 h组( IR 0 h组﹑IR 6 h组﹑IR 12 h组﹑IR 24 h组),每组6只。缺血再灌注组用无创性动脉夹夹闭左侧肾带,置于32℃温箱后1 h松开血管夹,随后切除右肾。 Sham组操作同上,但不夹闭左侧肾蒂。再灌注0﹑6﹑12﹑24 h后处死小鼠,收集肾脏及小鼠外周血标本。测定血肌酐(Cr)和尿素氮(BUN)水平。 PAS染色后显微镜下观察肾脏病理学变化, Western印迹和免疫组织化学法检测肾脏组织血管内皮生长因子受体3的表达。结果与Sham组相比较,再灌注0 h时小鼠血肌酐和尿素氮无明显升高,但缺血再灌注6﹑12﹑24 h后血肌酐和尿素氮呈显著性上升。 IR各组肾组织病理损伤也随着再灌注时间的延长而逐渐加重,可见肾小管上皮细胞明显肿胀坏死,蛋白管型形成,刷状缘脱落。随着缺血再灌注时间的进展, VEGFR-3蛋白表达量增加,免疫组织化学染色结果显示VEGFR3主要分布在肾脏皮质髓质交界处的肾小管。结论 VEGFR3在肾脏缺血再灌注损伤后表达量上升,且表达部位主要分布于肾脏皮髓质交界处的肾小管,因此VEGFR3可能参与调控肾脏缺血再灌注损伤。 相似文献
2.
目的:探讨兔肺缺血再灌注(I-R)中肺血管内皮细胞的损伤。方法:比较肺I-R和假手术对照组的血浆一氧化氮(NO)、内皮素-1(ET-1)及血气、肺水肿指标,分析肺脏超微结构。结果:I-R组血浆NO、ET-1水平显著高于假手术对照组,ET-1与动脉氧分压(PaO2)呈负相关,与肺湿/干重比呈正相关。再灌注期,PaO2明显低于对照组,肺湿/干重比明显高于对照组。电镜观察:缺血1h,肺毛细血管内皮细胞肿胀,Ⅰ型肺泡上皮细胞基膜增厚,Ⅱ型细胞微绒毛减少,板层小体减少,肺泡隔增厚。再灌注0.5h,毛细血管和肺泡上皮细胞损伤较明显,至再灌注2h结构开始修复。结论:I-R时肺毛细血管内皮细胞受损,其损伤可能在肺功能紊乱中起重要作用。 相似文献
3.
目的:探讨灯盏花素对肢体缺血再灌注骨骼肌的保护作用.方法:健康成年家兔20只,随机分为对照组和实验组,每组10只,建立兔肢体缺血再灌注损伤动物模型.在即将恢复血流灌注时,两组分别自耳缘静脉注射生理盐水(对照组)、灯盏花素注射液(实验组).分别在缺血前、缺血后2h,再灌注后1h、再灌注后3h采集术侧股静脉血样,测定血清乳酸脱氢酶(LDH)、肌酸激酶(CK)的含量.取上述各时相点动物胫前肌组织,测定骨骼肌组织湿/干重比值并观察肌组织微细和超微结构变化.结果:实验组再灌注后LDH、CK明显低于对照组(P<0.01),骨骼肌组织湿/干重比值低于同期对照组(P<0.05).光镜及电镜下观察实验组骨骼机损伤轻于对照组.结论:灯盏花素能够缓解组织水肿,保护缺血再灌注骨骼机. 相似文献
4.
严云珍 《四川生理科学杂志》2008,30(3):129-130
脑缺血再灌注损伤(Cerebra lischemia-reperfusion injury)是指缺血脑组织在恢复血液灌注后,脑组织损伤进一步加重的临床病理过程。灯盏花素是从灯盏花中分离出的一类黄酮类成分,主要含灯盏乙素(4,5,6-三羟基黄酮-7葡萄糖醛酸苷)、少量灯盏甲素及其他黄酮类成分。近年来的研究表明,灯盏花素对脑缺血再灌注后的脑损伤具有显著的保护作用,并已在临床应用中得到证实。本文就灯盏花素保护脑缺血再灌注损伤的作用机制作一综述。 相似文献
5.
血管内皮细胞生长因子与缺血性脑血管疾病 总被引:1,自引:0,他引:1
血管内皮细胞生长因子(VEGF)是内皮细胞特异性的有丝分裂原,在许多生理和病理过程中,具有增加血管通透性、促进新生血管形成等生物学功能,与缺血性脑血管疾病的发生、发展关系密切.本文着重介绍脑缺血时VEGF及其受体表达、细胞来源和生物学作用. 相似文献
6.
目的;研究犬小肠缺血再灌注后血管内皮细胞中的凋亡基因(Bcl-2,Bax)的血管内皮生长因子(VEGF)表达改变和意义。方法:阻断分布于小肠较小范围的小肠动脉,建立小肠缺血再灌注模型。以免疫组织化学方法对小肠组织中的Bcl-2,Bax和VEGF的表达进行观察研究。结果:小肠缺血再灌注后,Bcl-2,Bax和VEGF的表达有明显的改变。小肠再灌注0min,Bcl-2,Bax和VEGF的阳性细胞率分别为85%、55%和10%,再灌注30min ,分别为66%、54%和65%,而至再灌注60min,则分别为44%、75%和5%,在对照组仅有少量阳性细胞。结论:小肠缺血再灌注可引起抗凋亡基因Bcl表达夺加,但随着血流恢复而逐渐减少,而凋亡基因Bax的表达则逐渐增加。VEGF表达虽有一定增加,但最终减少。小肠缺血再灌注能增强调亡基因表达和诱导凋亡。 相似文献
7.
肾缺血再灌注损伤中微血管损伤防治的研究进展 总被引:6,自引:1,他引:6
随着肾移植、血管外科的建立和发展,使许多严重疾病的治疗,提高到了一个新的水平,而这些新方法所涉及的肾缺血再灌注损伤(ischemia-reperfusion injury,IRI),更引起国内外学者的高度重视。近年研究表明微血管损伤是IRI的重要发病机制之一。本文拟从微血管角度针对微血管血液流变性、微血管舒缩功能及通透性诸环节对肾 相似文献
8.
脂多糖对人脐静脉血管内皮细胞的直接损伤作用 总被引:1,自引:0,他引:1
血管内皮细胞 (endothelialcells,EC)炎症反应是感染性休克向不良方向演变的重要原因 ,有关激活剂 (LPS、IL 1)导致EC活化的研究是败血症病理反应的中心课题。内毒素引起微循环EC损伤是内毒素性组织损伤的重要环节之一。本实验探讨了LPS对体外培养脐静脉EC的直接损伤作用。1 材料与方法1 1 材料 :RMPI 16 40培养基、LPS(Sigma产品 )1 2 细胞培养及鉴定 :内皮细胞传 4代。PMN的分离采用Percoll’s分离液 5 0 0g离心 2 0min取白细胞层用培养基稀释成2× 10 6 mL备用。1 3 … 相似文献
9.
目的:观察体外模拟缺血/再灌注(ischemia/reperfusion,I/R)微环境下人肺微血管内皮细胞(human pulmonary microvascular endothelial cells,HPMVECs)的自噬变化,研究自噬在维持I/R条件下HPMVECs细胞存活及内皮屏障完整性中的作用。方法:用雷帕霉素(rapamycin,RAP)预处理HPMVECs,在缺糖缺氧/恢复糖和氧供(oxygen-glucose deprivation/oxygen-glucose restoration,OGD)模拟的I/R微环境中孵育细胞。应用Western blot及透射电镜法检测细胞自噬变化,用流式细胞术检测细胞凋亡,通透性小室法检测HPMVECs通透性。结果:OGD条件下HPMVECs的自噬水平明显升高,RAP预处理进一步上调了OGD条件下的细胞自噬。OGD组细胞凋亡率明显增高,细胞通透性增加。RAP预处理不仅降低了OGD引起的细胞凋亡率,而且减轻了OGD条件下细胞通透性。结论:自噬在I/R诱发的肺微血管内皮细胞损伤中发挥保护性作用,提高自噬水平有助于减少I/R条件下细胞凋亡并维持内皮屏障完整性。 相似文献
10.
目的:探讨实验大鼠眼缺血再灌注后葡萄膜组织中环氧合酶-2(COX-2)的表达及意义。方法:通过血管结扎法建立大鼠一侧眼缺血再灌注损伤模型,并以对侧眼作为假手术对照,检测实验眼分别缺血1h、2h、3h、4h、5h、6h情况下,脉络膜和虹膜组织中COX-2和血管内皮生长因子(VEGF)的表达。结果:在各组实验眼脉络膜和虹膜各层组织中都有不同程度COX-2和VEGF阳性表达,与假手术对照眼比较有显著性差异,P<0.01;且脉络膜或虹膜中COX-2和VEGF表达具有良好相关性,分别为r=0.943,r=0.886。结论:与炎症密切相关的COX-2可能作为潜在的血管增生刺激因子,在葡萄膜新生血管形成中起着重要作用。 相似文献
11.
Culture of human umbilical vein endothelial cells on immobilized vascular endothelial growth factor 总被引:1,自引:0,他引:1
Ito Y Hasuda H Terai H Kitajima T 《Journal of biomedical materials research. Part A》2005,74(4):659-665
Vascular endothelial growth factor (VEGF) was immobilized on substrata in photoreactive gelatin to control the adhesion and growth of vascular endothelial cells. The gelatin and VEGF were mixed in water and cast on a polystyrene dish or a silane-coated glass plate. The surface was then photoirradiated in the presence or absence of a photomask and washed. Toughness of the immobilized material was confirmed by ethanol treatment. Human umbilical vein endothelial cells (HUVECs) grew on the immobilized VEGF but not on a nontreated surface. Growth of HUVEC increased significantly with an increase in the amount of immobilized VEGF, and the effects were inhibited by treatment with anti-VEGF antibody. Thus, immobilized VEGF specifically interacted with HUVECs to permit growth in culture. Micropatterning of HUVEC cultures was also achieved using micropattern-immobilized VEGF. This patterning technique may be useful for the formation of blood vessel networks in vitro. 相似文献
12.
Baba Y Kato Y Mochimatsu I Nagashima Y Kurihara M Kawano T Taguchi T Hata R Tsukuda M 《Clinical & experimental metastasis》2004,21(5):419-425
Angiogenesis involves multiple steps including proliferation and migration of endothelial cells. In the present study, we determined the effect of inostamycin (an inhibitor of phosphatidylinositol synthesis) on vascular endothelial growth factor (VEGF)-induced proliferation and migration of human umbilical vein endothelial cells (HUVECs). Inostamycin significantly attenuated both VEGF-induced proliferation and migration of HUVECs. Inostamycin inhibited activation of mitogen-activated kinases (ERK and p38) and elevation of cyclin D1 induced by VEGF. These data suggest that inostamycin reduced both proliferation and migration of HUVECs by targeting ERK-cyclin D1 and p38, respectively. 相似文献
13.
目的:观察在培养条件下血小板活化因子(PAF)能否直接损伤原代人血管内皮细胞(HVEC)和ECV-304细胞系。方法:利用光镜和结晶紫比色的方法,观察HVEC、ECV-304细胞系与PAF孵育前后形态和生物活性变化。结果:PAF与HVEC孵育30min即发生细胞形态改变,生物活性则未见显著下降,与ECV-304细胞系孵育后的细胞形态和生物活性未见明显变化。结论:在培养条件下PAF可致HVEC损伤,对ECV-304细胞系则未见明显损伤。 相似文献
14.
目的:研究葡萄糖对人脐静脉内皮细胞蛋白C受体(EPCR)mRNA 表达的影响,以及吡格列酮的干预作用。方法:体外培养人脐静脉内皮细胞(HUVECs),分别以流式细胞术和RT-PCR技术确认HUVECs膜上EPCR的表达水平和 mRNA 水平的表达。再分别以含不同浓度D-葡萄糖(5、10、30、50 mmol/L)的培养基以及含吡格列酮(5、10、20 μmol/L)或不含吡格列酮的高糖(50 mmol/L)培养基孵育HUVECs 24 h,行剂量和时间依赖性实验,并采用实时定量PCR技术测定HUVECs细胞 EPCR mRNA 的表达。结果:随着培养基D-葡萄糖浓度的增加,HUVECs培养24 h后其EPCR mRNA 的表达逐渐下调。在采用吡格列酮干预后, 50 mmol/L高糖处理的HUVECs EPCR mRNA 表达的下调得到明显改善。结论:(1)EPCR 在HUVECs上高表达,高糖可通过下调EPCR mRNA 的表达而损伤内皮细胞功能。(2)吡格列酮可阻止高糖诱导的HUVECs EPCR mRNA表达的下调,从而保护内皮细胞功能。 相似文献
15.
P38信号通路在人脐静脉内皮细胞表达P-选择素中的作用 总被引:3,自引:2,他引:3
目的 :研究P38信号通路 (P38mitogen activatedproteinki nase ,P38MAPK)在人脐静脉内皮细胞表达P 选择素以及糖尿病动脉粥样硬化中的作用。方法 :分别以高葡萄糖、糖基化终产物 (AGE)、高胰岛素和过氧化氢刺激人脐静脉内皮细胞系ECV 30 4 ,再以P38MAPK特异性抑制剂SB2 0 35 80预处理 ,观察ECV 30 4细胞系中磷酸化P38MAPK和P 选择素的表达。结果 :4种刺激因素均可单独激活P38MAPK ,使磷酸化P38MAPK表达量明显增加 ,P 选择素表达量也明显增加 ;以SB2 0 35 80预处理后 ,P 选择素的表达被明显抑制。结论 :P38MAPK是P 选择素的上游信号分子 ,也可能是动脉粥样硬化发生的始动信号之一 相似文献
16.
目的:观察血管生成素4(Ang-4)对脂多糖(LPS)诱导的人脐静脉内皮细胞(HUVECs)损伤的影响,并探讨其可能的作用机制。方法:EnVision法免疫组化鉴定HUVECs。LPS诱导细胞损伤,不同剂量的Ang-4干预。显微镜下观察细胞形态,MTT法检测细胞活力,ELISA法检测von Willebrand因子(vWF)和肿瘤坏死因子(TNF-α)含量,real-time PCR检测Toll样受体4(TLR4)、核因子κB(NF-κB) p65和TNF-α mRNA含量变化。结果:免疫组化示胞浆内人Ⅷ因子相关抗原呈阳性;与正常组比,LPS组细胞增殖活力降低(P<0.01),vWF及TNF-α分泌增多(P<0.01),且TLR4、NF-κB p65和TNF-α mRNA表达升高(P<0.01);Ang-4(100 μg/L)组可恢复细胞活力,降低vWF及TNF-α含量(P<0.01),抑制LPS所致TLR4、NF-κB p65和TNF-α mRNA的表达(P<0.01)。结论:Ang-4可拮抗LPS诱导的HUVECs损伤,这可能与抑制TLR4-NF-κB p65-TNF-α信号通路的活化有关。 相似文献
17.
Aurora T. Alsop Jacquelyn C. Pence Daniel W. Weisgerber Brendan A.C. Harley Ryan C. Bailey 《Acta biomaterialia》2014,10(11):4715-4722
Biomolecular signals within the native extracellular matrix are complex, with bioactive factors found in both soluble and sequestered states. In the design of biomaterials for tissue engineering applications it is increasingly clear that new approaches are required to locally tailor the biomolecular environment surrounding cells within the matrix. One area of particular focus is strategies to improve the speed or quality of vascular ingrowth and remodeling. While the addition of soluble vascular endothelial growth factor (VEGF) has been shown to improve vascular response, strategies to immobilize such signals within a biomaterial offer the opportunity to optimize efficiency and to explore spatially defined patterning of such signals. Here we describe the use of benzophenone (BP) photolithography to decorate three-dimensional collagen-glycosaminoglycan (CG) scaffolds with VEGF in a spatially defined manner. In this effort we demonstrate functional patterning of a known agonist of vascular remodeling and directly observe phenotypic effects induced by this immobilized cue. VEGF was successfully patterned in both stripes and square motifs across the scaffold with high specificity (on:off pattern signal). The depth of patterning was determined to extend up to 500 μm into the scaffold microstructure. Notably, photopatterned VEGF retained native functionality as it was shown to induce morphological changes in human umbilical vein cells indicative of early vasculogenesis. Immobilized VEGF led to greater cell infiltration into the scaffold and the formation of immature vascular network structures. Ultimately, these results suggest that BP-mediated photolithography is a facile method to spatially control the presentation of instructive biological cues to cells within CG scaffolds. 相似文献
18.
蜕皮甾酮对肿瘤坏死因子致人脐静脉内皮细胞损伤的影响 总被引:9,自引:0,他引:9
目的和方法:实验以培养的人脐静脉内皮细胞(HUVEC)为研究对象,应用大剂量肿瘤坏死因子(TNF)造成HUVEC损伤,观察培养上清液血管紧张素转换酶(ACE)及HUVEC的超微结构变化,研究蜕皮甾酮(EDS)对内皮细胞损伤的影响。结果:大剂量TNF作用于HUVEC时,其培养上清液的ACE非常明显增高,超微结构破坏;应用EDS,则培养上清液的ACE有所减少、超微结构的损害程度有所减轻。结论:EDS能够减轻人血管内皮细胞的损伤,揭示了EDS在抗血管内皮细胞损伤方面的价值。 相似文献
19.
组织型纤溶酶原激活物(t-PA)在人体纤溶中起主导作用,与内皮细胞结合后可提高自身催化活性并免受其抑制物灭活。本实验用联胺诱发内皮细胞过氧化损伤,以硒做为抗氧化剂,用放射性核素测定及放射自显影的方法观察内皮细胞损伤前后与t-PA结合力的改变。结果表明:过氧化损伤后内皮细胞与t-PA结合力明显下降,硒对该结合力的下降有一定抑制作用。提示内皮细胞损伤后纤溶活性降低可能与二者结合力下降有关。 相似文献
20.
Early neutrophilic expression of vascular endothelial growth factor after traumatic brain injury 总被引:5,自引:0,他引:5
Chodobski A Chung I Koźniewska E Ivanenko T Chang W Harrington JF Duncan JA Szmydynger-Chodobska J 《Neuroscience》2003,122(4):853-867
The formation of edema after traumatic brain injury (TBI) is in part associated with the disruption of the blood-brain barrier. However, the molecular and cellular mechanisms underlying these phenomena have not been fully understood. One possible factor involved in edema formation is vascular endothelial growth factor (VEGF). This growth factor has previously been demonstrated to increase the blood-brain barrier permeability to the low molecular weight markers and macromolecules. In this study, we analyzed the temporal changes in VEGF expression after TBI in rats. In the intact brain, VEGF was expressed at relatively low levels and was found in the cells located close to the cerebrospinal fluid space. These were the astrocytes located under the ependyma and the pia-glial lining, as well as the epithelial cells of the choroid plexus. In addition, several groups of neurons, including those located in the frontoparietal cortex and in all hippocampal regions, were VEGF-positive. The pattern of VEGF-immunopositive staining of neurons and choroidal epithelium suggested that in these cells, VEGF binds to the cell membrane-associated heparan sulfate proteoglycans. Following TBI, there was an early (within 4 h post-injury) increase in VEGF expression in the traumatized parenchyma associated with neutrophilic invasion. The ipsilateral choroid plexus appeared to play a role in facilitating the migration of neutrophils from blood into the cerebrospinal fluid space, from where many of these cells infiltrated the brain parenchyma. VEGF-immunopositive staining of neutrophils resembled haloes and was found ipsilaterally within the frontoparietal cortex and around the velum interpositum, a part of the subarachnoid space. These haloes likely represent the deposition of neutrophil-derived VEGF within the extracellular matrix, from where this growth factor may be gradually released during an early post-traumatic period. The maximum number of VEGF-secreting neutrophils was observed between 8 h and 1 day after TBI. In addition, from 4 h post-TBI, there was a progressive increase in the number of VEGF-immunoreactive astrocytes in the ipsilateral frontoparietal cortex. The maximum number of astrocytes expressing VEGF was observed 4 days after TBI, and then the levels of astroglial VEGF expression declined gradually. Early invasion of brain parenchyma by VEGF-secreting neutrophils together with a delayed increase in astrocytic synthesis of this growth factor correlate with the biphasic opening of the blood-brain barrier and formation of edema previously observed after TBI. Therefore, these findings suggest that VEGF plays an important role in promoting the formation of post-traumatic brain edema. 相似文献