首页 > 文献资料
-
To observe the effects of essential garlic oil (EGO) on vascular cell adhesive molecule-1 (VCAM-1) expression of endothelial cells and monocyte-endothelial cell adhesion rate induced by interleukin-1α (IL-1α). Methods: Human umbilical vein endothelial cells (HUVEC) were isolated by trypsin digestion method and co-cultured with IL-1α or EGO+IL-1α in the absence or presence of U937 monocyte. Monocyte-endothelial cell adhesion rate was examined with reverted microscope. VCAM-1 expression of endothelial cells was measured by ACAS 570 confocal microscope, and the data were presented as mean fluorescent intensity. Results: EGO significantly inhibited IL-1α-induced endothelial expression of VCAM-1, and thus markedly decreased monocyte-endothelial cell adhesion rate. Conclusion: EGO has the effect on antagonizing adhesion of monocyte and vascular endothelial cell, which might be due to its inhibition on adhesive molecular expression on the surface of endothelial cells.
-
益气活血通络中药对不稳定型心绞痛患者循环内皮细胞的影响
有研究发现,血管内皮细胞(vascular endothelial cells, VEC)功能障碍在动脉粥样硬化和冠心病的发生、发展中起重要作用,众多的冠心病危险因素往往是以损伤内皮细胞而起致病作用的.
-
Liver fibrosis is a gradual process of increased secretion and decreased degradation of extracellular materials (ECM). Most author hold that the process is initiated by the damage of hepatic cells (HCs), which leads to activation and secretion of multiple cellular factors of Kupffer cells. These factors, along with the cellular factors secreted by damaged HCs, thrombocytes and endothelial cells of the hepatic sinusoid, and some chemical mediators are activators of hepatic stellate cells (HSCs). Being activated, HSCs differentiate into myofibroblasts, and, via self-secretion and parasecretion, proliferate and synthesize a massive amount of extracellular materials which gradually accumulate and lead to formation of liver fibrosis.1 Since fibrosis is a common course in a variety of chronic liver diseases, prevention against its formation is of great importance. The following are the recent achievements of traditional Chinese medicine (TCM) in this field.
-
Ox-LDL增加人脐静脉内皮细胞分泌白三烯C4
氧化型低密度脂蛋白(oxidized low density lipoprotein,ox-LDL)是动脉粥样硬化(atherosclerosis,AS)重要的危险因素之一.它可以直接损伤内皮细胞,也可刺激内皮细胞表达大量的黏附分子、趋化因子,促使单核细胞黏附于内皮细胞、趋化单核细胞进入内膜和促进泡沫细胞形成,从而导致AS的发生.
-
氧化修饰减弱HDL上调人脐静脉内皮细胞ABCA1表达
血脂异常是动脉粥样硬化(atherosclerosis,AS)的始动性因素.血浆高密度脂蛋白(high density lipoprotein,HDL.)在体内能被多种因素氧化,其抗AS的作用随之减弱.
-
川崎病急性期患儿血清活化HUVECs NF-κB并促进MMP-9分泌
川崎病( Kawasaki disease ,KD),又称皮肤黏膜淋巴结综合征( mucocutaneous lymph node syndrome , MCLS ),是一种好发于5岁以下儿童和婴幼儿的急性全身性血管炎性疾病。病变可累及动脉、静脉和毛细血管,尤以冠状动脉为明显,成为小儿后天性心脏病的主要病因[1]。目前,KD病因与发病机制尚不十分清楚,本实验观察川崎病患儿急性期血清对人脐静脉内皮细胞( human umbilical vein endothelial cells , HUVECs ) NF-κB P65表达及MMP-9分泌的影响,及NF-κB抑制剂四氢化吡咯二硫代氨基甲酸脂( PDTC)对上述过程的影响。
-
TGFβ1在体外培养人淋巴管内皮细胞的表达
内皮细胞具有活跃的代谢功能,血管内皮细胞合成和分泌功能已多有研究和评述,相比较而言,同属于内皮的淋巴管内皮细胞生物学功能却知之甚少.转化生长因子β1(TGFβ1)是一种多功能细胞因子,除了刺激多种细胞因子、炎性介质等合成分泌外,还影响肿瘤的形成和发展.近来研究表明淋巴管内皮细胞与肿瘤细胞的转移有关[1].本实验即以人淋巴管内皮细胞为研究对象,观察TGFβ1在其中的表汰.
-
β-NGF减轻H2 O2对HUVECs的损伤
血管内皮细胞损伤被认为是导致动脉粥样硬化的重要病理原因之一,且多与氧化应激损伤有关。因此,如何保护氧化损伤后血管内皮细胞功能对于防治动脉粥样硬化等心血管疾病具有重要意义。神经生长因子β-NGF是一种多功能性神经营养因子,可以促进血管新生且与血管内皮功能密切相关,但其对氧化损伤后血管内皮细胞的作用及其机制尚未知[1]。因此本研究以人脐静脉血管内皮细胞( human um-bilical vein endothelial cells , HUVECs )为研究对象,利用H2 O2诱导其氧化损伤进而研究β-NGF对血管内皮细胞的保护作用及其机制。
-
脂多糖对人脐静脉血管内皮细胞的直接损伤作用
血管内皮细胞(endothelial cells,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.
-
大鼠脊髓微血管内皮细胞的分离培养与鉴定
脊髓微血管内皮细胞(spinal cord microvascular endothelial cells,SCMECs)参与构成血脊髓屏障,其功能变化与多种脊髓相关疾病相关.目前分离SCMECs的文献很少.本研究拟基于分离多种原代内皮细胞的经验[1-2],建立分离纯化SCMECs的方法.1 材料与方法1.1 材料1.1.1 试剂:DMEM(高糖)、胎牛血清(FBS)、Ⅱ型胶原蛋白酶、双抗、庆大霉素、谷氨酰胺和l×PBS(北京协和医学院细胞中心);牛血清白蛋白(bovine serum albumin,BSA)、胶原蛋白酶/分散酶(collagenase/dispase)(Roche公司);嘌呤霉素(Sigma公司);内皮细胞培养基(ECM)(Scien Cell公司);兔抗大鼠yon Willebrand factor(vWF)抗体(SantaCruz公司);抗GFAP抗体和抗α-SMA抗体(Abcam公司);FITC标记和TRITC标记的二抗(北京中衫金桥公司).
-
多肽类物质在体外培养星形胶质细胞中的表达
Recently, scientists interested in the diseases of human brain have paid much attention to the neuropeptides [Nie XJ, et al. Rev Neurosci 1996, 7(3): 177]. Under normal conditions, these neuropeptides are found in some types of neurons and in endothelial cells of microvessels but not in glial cells.
-
大鼠肾小球内皮细胞分离培养和鉴定
一、材料和方法1.材料和试剂:(1)材料:SD大鼠1~2月龄,体重50~100 g,雌雄各半,由东南大学医学院实验动物中心提供.Mini MACS免疫磁珠细胞分选仪、磁性分离柱LS 购自Miltenyi Biotec公司.(2)试剂:Ⅳ型胶原酶、内皮细胞生长因子、胰蛋白酶及转铁蛋白均购自Sigma公司,DMEM培养基购自Gibco公司,异硫氰酸荧光素标记的抗CD34-FITC、抗波形蛋白及抗角蛋白均购自Santa Cruz公司,抗FITC免疫磁珠购自Miltenyi Biotec公司.
-
Objective:Blood-brain barrier is the key barrier of brain in the innate immune. It can prevent the harmful substances from the blood into the brain. In order to keep the brain in a relatively stable environment and maintain the normal function of the nervous system, it can also pump harmful substances or excess substances outside the brain selectively. Among them, brain microvascular endothelial cell tissue is a key part in the blood-brain barrier's function. The number of the patients with central nervous system ( CNS) diseases increased year by year. The therapeutic drug is usually inhibited by the blood-brain barrier and is difficult to work. Therefore, how to modify the drug and to make it easier to cross the blood brain barrier is the key point to cure CNS. At present, more than 95% research focus only on how nano drugs can enter the cell, the way and efficiency to enter the cell and the research of effect of nano drug etc. For the process of drug carrier in endocytosis, intracellular transport and release and regulation of research are rarely reported. Clathrin and P-glycoprotein are related protein in endo-cytosis and exocytosis with nano drug. Clathrin is located on the plasma membrane. It participates in endocytosis of some nutrients, and maybe the entry into the cell of some drugs. P-glycoprotein is located in the membrane of cer-ebral capillary endothelial cells. It can efflux drugs relying on ATP. Although there is a certain understanding of the cell in the inner swallow and efflux. But the process of the liposome drug is not clear. To solve the above prob-lems, using colloidal gold liposome nano materials to trace liposome's transport and regulation mechanism in brain microvascular endothelial cells, and study endocytosis, release, distribution and regulation mechanism of nano lipo-somes in brain microvascular. The solution of this problem can guide to construct reasonable drug carrier, and look forward to clarifing the molecular basis and mechanism of nano drug carriers across the BBB. This work has impor-tant theoretical and practical significance for the development and application of liposomes in the future. Results:For untreated cerebral microvascular endothelial cells, the cells incubated with colloidal gold liposomes can uptake of liposome colloidal gold, and with the extension of time, there are gold colloids in the plasma membrane, endo-plasmic reticulum, Golgi apparatus and lysosomes in order, and finally colloidal gold liposome exports out of the cell. For cerebral microvascular endothelial cells treated by sodium azide, compared with untreated cells, the cells incubated with colloidal gold liposomes, cannot be observed liposome colloidal gold in them. For cerebral microvas-cular endothelial cells treated by reserpine, the cells incubated with colloidal gold liposomes, compared with un-treated cells, colloidal gold liposome cannot export out of the cell. Conclusions:The uptake of liposomes in brain microvascular endothelial cells require clathrin's participation. The excretion of liposomes from brain microvascular endothelial cells require P-glycoprotein's participation. After colloidal gold liposome entering brain microvascular endothelial cells, it moves into the endoplasmic reticulum, Golgi apparatus and lysosomes in order. Finally colloi-dal gold liposome exports out of the cell.
-
内皮祖细胞与缺血性脑血管病研究进展
脑卒中是严重危害人类健康的疾病,其中缺血性脑卒中占了80%左右.3 h超早期用组织型纤溶酶原激活剂(t-PA)溶栓,由于受时间窗及其本身溶栓成功率的限制,只有约2%~3%缺血性脑卒中患者得到了溶栓治疗[1],内皮祖细胞(endothelial progenitor cells,EPCs)的发现有可能为缺血性脑血管病的治疗提供一种全新的有希望的治疗方法.EPCs已经成功地在外周血、骨髓、脐血、血管壁、以及其他一些组织器官中分离出,并被证实其主要参与血管动态维持和生理性重建[2].
-
淋巴管新生机制与调节的研究进展
淋巴管系统作为除血管系统外的人体第二套循环系统,起到调节体液平衡、运送组织间隙的蛋白质以及免疫等功能.尽管淋巴管系统和血管系统相互依赖以维持内环境稳定,但它们在结构和功能方面存在着明显的差别.在以往的研究中,有关血管发育和新生的调节机制颇受重视,取得了很大的进展,而对淋巴系统的研究一直局限于解剖学层面.随着近年来对淋巴管内皮细胞(lymphatic endothelial cells,LECs)分离纯化技术的发展和对其特有分子标志和分子特性的深入了解,这一现象正在迅速得到改观.尤其是淋巴管发育和新生的机制及其调节在特定的先天性异常如淋巴水肿,以及肿瘤的淋巴道转移等病理现象中起重要作用,因此该领域的研究对阐明相关疾病的发病机理甚至治疗应用都非常重要.
-
Objective: To analyze the expression of inducible nitric oxide synthase (iNOS), endothelial nitric oxide synthase (eNOS) and vascular endothelial growth factor (VEGF) in hepatocellular carcinoma (HCC) and its relation to angiogenesis. Methods: Tissue sections from 71 HCC patients were examined immunohistochemically for protein expression of iNOS, eNOS, and VEGF. Microvessal density (MVD) was counted by endothelial cells immunostained by anti-CD34 antibody. Results: Positive immunostaining for iNOS, eNOS was detected in 83.1% and 85.9% of HCC respectively. INOS and eNOS were not detected in normal hepatic tissue. MVD was 34.3±1.5/HP and 38.6±1.6/HP in HCC with positive staining for iNOS and VEGF while it was 31.2± 2.8/HP, and 22.4± 2.0/HP in HCC with negative staining for iNOS and VEGF (P<0.01). A correlation between NOS expression and VEGF in HCC was not observed. Conclusion: iNOS and eNOS may play a role in malignant transformation f post-hepatic cirrhosis. The expression of iNOS and VEGF favors angiogenesis of HCC.
-
胰岛素通过内皮与平滑肌细胞改变小鼠的脑血管功能
胰岛素对于颅内动脉的影响尚无相关研究.Prasad Venkateswera Gurunath Katakam,et al研究通过聚合酶链反应(polymerase chain reaction,PCR)及免疫印迹的方法证实胰岛素受体在脑血管及培养的微血管内皮细胞中表达(cerebral microvascular endothelial cells,CMVECs),通过监测血管直径发现胰岛素作用的双相性:在0.1 ng/ml(-9.7%+1.6%)时收缩血管,在1~100 ng/ml(31.9%+1.4%)时扩张血管.
-
Objective.To investigate the effect of peroxisome proliferator activated receptors (PPARs) activators on plasminogen activator inhibitor type 1 (PAI 1) expression in human umbilical vein endothelial cells and the possible mechanism.Methods.Human umbilical vein endothelial cells (HUVECs) were obtained from normal fetus,and cultured conventionally.Then the HUVECs were exposed to test agents (linolenic acid,linoleic acid,oleic acid,stearic acid and prostaglandin J2 respectively) in varying concentrations with fresh media.RT- PCR and ELISA were applied to determine the expression of PPARs and PAI 1 in HUVECs.Results.PPAR α,PPAR δ and PPAR γ mRNA were detected by using RT PCR in HUVECs.Treatment of HUVECs with PPARα and PPAR γ activators- - linolenic acid,linoleic acid,oleic acid and prostaglandin J2 respectively,but not with stearic acid could augment PAI I mRNA expression and protein secretion in a concentration dependent manner.However,the mRNA expressions of 3 subclasses of PPAR with their activators in HUVECs were not changed compared with controls.Conclusion.HUVECs express PPARs.PPARs activators may increase PAI 1 expression in ECs,but the underlying mechanism remains unclear.Although PPARs expression was not enhanced after stimulated by their activators in ECs,the role of functionally active PPARs in regulating PAI 1 expression in ECs needs to be further investigated by using transient gene transfection assay.
-
急性缺氧对冠状动脉内皮细胞释放ET-1、NO、PGI2的影响
冠状动脉内皮细胞能分泌多种血管收缩和舒张物质.其中缩血管物质以内皮素的缩血管作用强,且作用持久.内皮源性舒张因子主要为NO和花生四烯酸代谢产物PGI2.三种内皮源性血管活性因子均通过旁分泌方式作用于血管内皮下的平滑肌细胞,调节局部血管紧张度和血流量.在体研究表明缺氧可引起内皮素-1、NO、PGI2合成分泌改变.但在体研究时血浆及组织匀浆中ET-1、NO、PGI2的浓度改变难以反映其在血管内皮细胞形成和释放的状况.国外有关缺氧对离体冠状动脉内皮细胞合成和释放ET-1、NO、PGI2影响的研究也才刚起步,缺氧时间短暂,时相点少.国内尚未见报道.因此我们建立了离体内皮细胞缺氧模型,观察了多个时间点缺氧对冠状动脉内皮细胞释放ET-1、NO、PGI2的影响.
-
褪黑素对人脂肪来源的间充质干细胞向内皮细胞分化的促进作用研究
人脂肪来源的间充质干细胞(hADSC)是人脂肪组织中不同成熟阶段的脂肪前体细胞中分化程度差的一种,具有生物学特性稳定、来源充足、体外培养条件要求低、扩增能力强等特点,是组织工程化的优秀种子细胞.褪黑素是一种具有较强自由基清除功能的吲哚类激素.褪黑素不但对血管内皮细胞(EC)的损伤有保护作用,且可以促进EC的增殖[1-2].我们拟研究褪黑素对hADSC分化为EC过程的作用,并观察该过程中细胞内游离钙离子([Ca2+]i)的变化以及对细胞外调节激酶/ERK/MAPK信号通路的影响.