非霍奇金淋巴瘤患者sVEGF和sbFGF水平的变化及临床意义

目的:研究非霍奇金淋巴瘤(NHL)患者血清血管内皮生长因子(sVEGF)及血清碱性成纤维细胞生长因子(sbFGF)水平与临床特征的关系,探索其临床意义.方法:ELISA法检测36例不同病期NHL患者sVEGF、sbFGF水平,并收集临床资料,进行统计分析.结果:NHL患者sVEGF、sbFGF水平明显高于对照组(均P＜...     

血管内皮生长因子调节内皮祖细胞生物学功能

目的研究血管内皮生长因子（VEGF）对体外培养骨髓源性内皮祖细胞（EPCs）数量及增殖、迁移、黏附功能的影响及机制初探。方法密度梯度离心法获取骨髓单个核细胞,FITC-荆豆凝集素I、DiI-乙酰化低密度脂蛋白荧光双染鉴定。单个核细胞培养7d后分为对照组和VEGF干预组。VEGF干预组加入不同浓度VEGF（25,50,75,100μg／L）培养48h,分别采用四氮唑溴盐比色法、改良的Boyden小室和黏附能力测定观察EPCs的增殖、迁移和黏附能力。RT—PCR法半定量检测VEGF对EPCs内皮型一氧化氮合酶（eNOS）mRNA表达的影响。硝酸还原酶法比色测定VEGF对EPCs分泌一氧化氮的影响。结果VEGF可浓度依赖性地增加EPCs数量并明显促进EPCs的黏附、迁移和增殖能力,与对照组比较差异显著。VEGF可上调EPCseNOSmRNA的表达,促进EPCs分泌一氧化氮。结论VEGF可能通过上调EPCseNOSmRNA的表达影响EPCs部分生物学功能。     

胃癌组织与血清中VEGF和bFGF的表达意义

目的：研究胃癌患者血清和组织中VEGF,bFGF的表达与胃癌临床特征之间的关系,研究二者的相关性及组织和血清之间的相关性,探讨VEGF,bFGF在胃癌的发生、发展、侵袭和转移中的作用方法：应用酶联免疫技术(ABC-ELISA方法)检测73例胃癌患者术前血清和20例健康体检者血清中的VEGF,bFGF的表达水平,同时应用免疫组织化学染色方法检测癌组织和癌旁组织中VEGF,bFGF的表达．结果：胃癌患者术前血清VEGF,bFGF表达水平均明显高于健康体检者(YEGF：101．8±53．3 ng/L vs 16．1±22．5ng/L,P＜0．05；bFGF：152．9±42．7ng/L vs 25．0±11．4ng/L,P＜0．05)．胃癌患者术前血清VEGF,bFGF的表达水平均随胃癌的浸润深度、TNM分期、淋巴结转移、远处转移而增高(P＜0．05),而与年龄、性别及病理类型无关．胃癌组织VEGF的阳性表达率为71．2%,癌旁组织中VEGF均未见阳性表达,二者之间有显著性差异(X~2=32．1,P＜0．05)；胃癌组织中bFGF的阳性表达率为63．0%、癌旁组织中bFGF阳性表达率为(10%),二者之间亦有显著性差异(X~2=17．7,P＜0．05)．胃癌患者组织VEGF,bFGF的表达水平均与胃癌的浸润深度、TNM分期、淋巴结转移、远处转移有关(P＜0．05),而与年龄、性别及病理类型无关．胃癌患者血清VEGF的表达水平与血清bFGF的表达水平呈明显正相关(r=0．439,P＜0．01),胃癌患者组织VEGF的表达水平与组织bFGF的表达水平呈明显正相关(r=0．391,P＜0．01)；胃癌患者术前血清VEGF的表达水平与组织VEGF的表达呈正相关(r=0．346,P＜0．01),术前血清bFGF的表达水平与组织bFGF的表达呈正相关(r=0．304,P＜0．01),均有显著性差异．结论：VEGF,bFGF在胃癌的发生、发展、转移及预后起着重要的作用,有望成为胃癌术前诊断、术后随访、复发转移监测、评价抗血管生成药物疗效和化疗效果判定的新的肿瘤标志物．     

The crucial role of vascular permeability factor/vascular endothelial growth factor in angiogenesis: a historical review

Angiogenesis is a biological process by which new capillaries are formed and it occurs in many physiological and pathological conditions. It is controlled by the net balance between molecules that have positive and negative regulatory activity and this concept had led to the notion of the 'angiogenic switch', depending on an increased production of one or more of the positive regulators of angiogenesis. Numerous inducers of angiogenesis have been identified and this review offers a historical account of the relevant literature concerning the discovery of one of the best characterized angiogenic factors, namely vascular endothelial growth factor (VEGF)/vascular permeability factor. Moreover, different strategies, designed to stimulate and to inhibit VEGF production in the context of several potential therapeutical implications, are discussed.     

大鼠静脉血栓栓塞症血管内皮生长因子和碱性成纤维细胞生长因子的研究

目的建立大鼠静脉血栓栓塞症（VTE）模型,观察大鼠VTE后血管内皮生长因子（VEGF）和碱性成纤维细胞生长因子（bFGF）的变化。方法sD大鼠78只,随机分为DVT（18只）、DVT-PTE（54只）、正常对照（6只）组。DVT组依据血栓形成时间不同（1,4,7d）分为D1、D4、D7三个亚组;DVT-PTE组依据DVT和PTE时间不同（1,4,7d）分为D1P1、D1P4、D1P7、D4P1、D4P4、D4P7、D7P1、D7P4、D7P7九个亚组,每亚组6只。采用显微血管夹阻滞一侧股静脉血流,制备DVT模型;DVT后不同时间分离有血栓的股静脉,摘取血栓,从另一侧股静脉注入栓子,制备DVT-PTE模型。行肺组织VEGF和bFGF免疫组织化学检查,并测定血浆VEGF和bFGF浓度。结果1、VEGF抗原：对照组主要在支气管上皮细胞胞浆表达,DVT-PTE组第1天肺动脉平滑肌细胞和肺泡上皮细胞胞浆可见表达,第4天肺动脉内皮细胞胞浆可见表达,第4和7天机化栓子中成纤维细胞胞浆有表达。bFGF抗原：对照组主要由支气管平滑肌和肺动脉平滑肌细胞胞浆表达,DVT-VIE组第1天肺动脉平滑肌细胞胞浆表达增强,第4和7天肺动脉周围基质和机化栓子内成纤维细胞胞浆可见表达。2、血清bFGF浓度在D1亚组升高,而在D7、D7P4和D7P7亚组降低,与对照组比较差异均有显著性（P〈0.05）。结论VEGF和bFGF参与VTE血栓机化和血管内膜修复。     

The effect of antibody against vascular endothelial growth factor on tumor growth and metastasis

Vascular endothelial growth factor (VEGF), a very important in the process of tumor angiogenesis, was chosen as a target in a study to determine whether manipulation of angiogenesis with antibody against VEGF may interrupt tumor growth and metastasis. Anti-VEGF antibody was obtained from immunized rabbits, purified on an affinity column, and identified as neutralized antibody by Mile's assay. IVTA₂MA891, a murine spontaneous breast cancer with a high rate of metastasis in lung in TA₂ × 615 F1 mice, was chosen as an animal model in this study, because of the high expression of VEGF in the primary tumor as well as in the lung metastatic tumor. The anti-VEGF antibody could inhibit growth of S180 sarcoma in a dose-dependent manner, and the inhibition rate could reach 41.0% with a dose of 200 μg mouse⁻¹ day⁻¹. Anti-VEGF antibody could inhibit tumor growth by 76.2% in nude mice bearing human gastric cancer (MGC 803). When anti-VEGF antibody was combined with ¹³¹I-3H11, a murine monoclonal antibody conjugated with ¹³¹I, only one of five nude mice developed tumor and 84.0% more inhibition of tumor growth was obtained in comparison with treatment by ¹³¹I-3H11 alone. The growth of the primary tumor was inhibited by 44.0% and the number and size of the metastatic foci in the lungs were reduced by 73.0% and 83.7% respectively in the animal model, with a high rate of metastasis in lung. The anti-VEGF antibody may be potentially useful for clinical treatment of cancer and metastasis. Received: 2 January 1998 / Accepted: 17 March 1998     

Serum levels of the angiogenic cytokines basic fibroblast growth factor (bFGF), vascular endothelial growth factor (VEGF) and hepatocyte growth factor (HGF) in multiple myeloma

Angiogenesis is a crucial process in growth and progression of cancer and there is growing evidence that neovascularisation is important in hematological malignancies. Since an increased angiogenic potential has been identified in multiple myeloma, we simultaneously measured circulating serum levels of the cytokines bFGF, VEGF, HGF and IL-6 by ELISA in 67 patients with multiple myeloma or monoclonal gammopathies of undetermined significance (MGUS) and in 20 controls. Median values of bFGF were 4.7 pg/ml in healthy volunteers, 6.2 in MGUS, 6.3 in myeloma stage I, 13.4 in stage II and 21.7 in stage III. Myeloma patients had significantly higher bFGF serum levels than controls (p<0.001). Pretreatment bFGF levels differed significantly in the Salmon and Durie stages I-III (p=0.02) and were significantly elevated in stage II-III compared to stage I myeloma (p=0.02). In patients responding to chemotherapy according to the CLMTF criteria, a significant decrease in serum bFGF, VEGF and HGF levels occurred (median pretreatment values for bFGF 23.9 pg/ml, post-treatment 6.5 pg/ml; p<0.001, for VEGF 223 pg/ml versus 105 pg/ml; p=0.02 and for HGF 1429 pg/ml versus 1077 pg/ml; p=0.02, respectively). In 11 patients who did not achieve a remission, there was no significant decrease in bFGF, VEGF and HGF levels. These data show that myeloma in stages II and III is associated with an increase in serum bFGF concentrations and give the first report that effective chemo-therapy is accompanied by a significant decrease in the angiogenic factors bFGF, VEGF and HGF, while no decrease of these factors could be found in nonresponders.     

MSCs transfected with hepatocyte growth factor or vascular endothelial growth factor improve cardiac function in the infarcted porcine heart by increasing angiogenesis and reducing fibrosis

Background

Cell transplantation and gene therapy have been demonstrated to have beneficial effects after a myocardial infarction (MI). Here, we used a large animal model of MI to investigate the beneficial effects of mesenchymal stem cells (MSCs) transfected with hepatocyte growth factor (HGF) or vascular endothelial growth factor (VEGF) genes.

Methods

A porcine MI model was created by balloon occlusion of the distal left anterior descending artery for 90 min followed by reperfusion. At 1 week after MI, the pigs were infused via the coronary vein with saline (n = 8), MSCs + AdNull(n = 8), MSC + VEGF(n = 10), or MSC + HGF(n = 10). Cardiac function and myocardial perfusion were evaluated by using echocardiography and gated cardiac perfusion imaging before and 4 weeks after transplantation. Morphometric and histological analyses were performed.

Results

All cell-implanted groups had better cardiac function than the saline control group. There were further functional improvements in the MSC + HGF group, accompanied by smaller infarct sizes, increased cell survival, and less collagen deposition. Blood vessel densities in the damaged area and cardiac perfusion were significantly greater in the MSC + AdNull group than in the saline control group, and further increased in the MSC + VEGF/HGF groups. Tissue fibrosis was significantly less extensive in the MSC and MSC + VEGF groups than in the saline control group and was most reduced in the MSC + HGF group.

Conclusion

MSCs (alone or transfected with VEGF/HGF) delivered into the infarcted porcine heart via the coronary vein improved cardiac function and perfusion, probably by increasing angiogenesis and reducing fibrosis. MSC + HGF was superior to MSC + VEGF, possibly owing to its enhanced antifibrotic effect.     

Endothelial cells overexpressing basic fibroblast growth factor (FGF-2) induce vascular tumors in immunodeficient mice

Basic fibroblast growth factor (FGF-2) is expressed in vascular endothelium during tumor neovascularization and angioproliferative diseases, including vascular tumors and Kaposi's sarcoma (KS). We have investigated the in vivo biological consequences of endothelial cell activation by endogenous FGF-2 in a mouse aortic endothelial cell line transfected with a retroviral expression vector harboring a human FGF-2 cDNA and the neomycin resistance gene. FGF-2 transfectants, named pZipbFGF2-MAE cells, caused the rapid growth of highly vascularized, non-infiltrating tumors when injected in nude mice. In contrast, lesions grew poorly when cells were injected in immunocompetent syngeneic animals. Histologically, the tumors had the appearance of hemangioendothelioma with spindled areas resembling KS and with numerous CD31+ blood vessels and lacunae. Southern blot analysis of tumor DNA, as well as disaggregation of the lesion followed by in vitro cell culture, revealed that less than 10% of the cells in the tumor mass retain FGF-2 overexpression and neomycin resistance at 6–8 weeks post-injection. Nevertheless, in vitro G418 selection allowed the isolation from the tumor of a FGF-2-overexpressing cell population showing biochemical and biological characteristics similar to those of pZipbFGF2-MAE cells, including the capacity to originate vascular lesions when re-injected in nude mice. To evaluate the effect of angiostatic compounds on the growth and vascularization of pZipbFGF2-MAE cell-induced lesions, nude mice were treated weekly (100mg/kg, i.p.) with the angiostatic sulfonated distamycin A derivative 2,2-(carbonyl-bis-[imino-N-methyl-4,2-pyrrole carbonyl-imino-{N-methyl-4,2-pyrrole}carbonylimino])-bis-(1,5-naphthalene) disulfonic acid (PNU 153429). The results demonstrate that PNU 153429 inhibits the growth of the lesions and causes a 50% decrease in CD31+ microvessel density. In conclusion, the data indicate that FGF-2-overexpressing endothelial cells cause vascular lesions in immunodeficient mice which may represent a novel model for opportunistic vascular tumors suitable for the evaluation of angiostatic compounds.     

Effect of glycation on basic fibroblast growth factor induced angiogenesis and activation of associated signal transduction pathways in vascular endothelial cells: possible relevance to wound healing in diabetes

Ineffectual wound healing in hyperglycaemic patients suffering from diabetes mellitus is characterised by a reduction in capillary reformation (angiogenesis). Basic fibroblast growth factor (FGF-2) is secreted by fibroblasts, macrophages and in particular endothelial cells (EC) in response to tissue injury and is important in promotion of neovascularisation. Recently, glycation of FGF-2 has been shown to significantly reduce its activity in vitro. We have examined the kinetics of FGF-2 glycation and compared its ability with that of native FGF-2 to activate mitogenesis, capillary formation and associated signal transduction in bovine aortic EC (BAEC). FGF-2 was exposed to 0.25 M glucose-6-phosphate (G-6-P) for 24–72 h and the degree of glycation determined by matrix assisted laser desorption ionisation mass spectrometry. Native FGF-2 was heterogeneous with Mw in the range 15,153.6–17,903 Da. After 24 h incubation with G-6-P there was evidence of glycation, and the mass increase corresponded to addition of 2.7 mol of G-6-P residues; after 48 h, 4 mol sugar was added and this increased to 8.7 after 72 h. Dimerisation of FGF-2 was observed after 72 h of treatment. Induction of mitogenesis in BAEC was significantly reduced by 25%–40% after treatment for 48–96 h with glycated (24 h) FGF-2 (gFGF-2;100 pg/ml–5 ng/ml; P < 0.05), whilst capillary tubule formation was significantly reduced by between 60% and 90% (100 pg/ml–1 ng/ml; P < 0.05) after 5 days compared to native FGF-2. Subsequent investigation of the signal transduction molecules associated with mitogenesis showed a reduction in FGF-2 induced tyrosine phosphorylated proteins of approximate Mw 20–150 kDa between 10 min and 24 h, in particular, mitogen activated protein kinase (MAPK)/early response kinase (ERK-1, ERK-2), after glycation. To determine the reason for reduced angiogenic activity of gFGF-2, we compared its binding characteristics to that of native FGF-2. Total binding of gFGF-2 to the cell surface was significantly reduced in BAEC analysed by FACS compared to native FGF-2 (P < 0.05). Further investigation using ¹²⁵I-labelled differentially washed samples, demonstrated a significant reduction in gFGF-2 binding to the high affinity tyrosine kinase receptor (46%) compared to native FGF-2. In summary, glycation of FGF-2 in vitro occurs rapidly within 24 h in the presence of elevated levels of G-6-P. Glycation caused a significant reduction in the ability of FGF-2 to bind to the tyrosine kinase receptor and activate signal transduction pathways responsible for both mitogenesis and capillary formation in BAEC. These results could help to explain the mechanism behind impaired wound healing in patients with diabetes mellitus. This revised version was published online in June 2006 with corrections to the Cover Date.     

血管、淋巴管内皮生长因子在胰腺癌中的表达

研究血管内皮生长因子(VEGF)在胰腺癌中的表达及意义,采用:Northern blot分析法检测正常胰腺组织和胰腺癌组织中VEGF-A、c mRNA的表达;采用免疫组织化学染色法检测胰腺癌标本中VEGF-A、C蛋白的表达。结果发现胰腺癌组织中VEGF-A和VEGF-C基因的表达分别是正常胰腺组织中的3.0和3.6倍;免疫组织化学染色法显示胰腺癌组织中VEGF-A和VEGF-C的阳性率分别为50％和80％;胰腺癌细胞VEGF-A的表达与肿瘤大小呈正相关,VEGF-C的表达与淋巴结转移呈正相关,均有统计学意义(P<0.05),而VEGF-A与VEGF-C表达无关联。胰腺癌非同步联合表达血管和淋巴管内皮生长因子,前者与肿瘤大小、局部范围相关联,后者与淋巴结转移相关联。     

血管内皮、碱性成纤维细胞生长因子表达与非小细胞肺癌患者生存期的关系

目的 探讨血管内皮生长因子(VEGF)、碱性成纤维细胞生长因子(bFGF)在非小细胞肺癌(NSCLC)中的表达及其与患者生存期的关系。方法 应用免疫组织化学方法检测96例NSCLC组织中VEGF、bFGF蛋白水平的表达，并探讨二者表达与患者生存期的关系。结果 NSCLC中VEGF、bFGF表达阳性率分别为51．0％(49／96)和58．3％(56／96)，二者具有相关性(P=0．041)，与患者生存期之间无统计学意义。结论 VEGF、bFGF在NSCLC血管形成中起重要作用，但不是NSCLC独立的预后因素。     

Role of vascular endothelial growth factor in angiodysplasia: an interventional study with thalidomide

Background and Aim: The pathogenesis of angiodysplasia is still not fully understood and effective therapy is not available. Thalidomide was reported to be effective in the treatment of angiodysplasia, but the mechanisms underlying its activity are, as yet, unknown. We aimed to investigate the expression of vascular endothelial growth factor (VEGF) in angiodysplasia tissues, and the role of hypoxia‐inducible factor‐1α (HIF‐1α) and basic fibroblast growth factor (bFGF) on VEGF expression in human umbilical vein endothelial cells (HUVEC). Additionally, we aimed to study the role of thalidomide in these parameters. Methods: Immunohistochemistry was performed to visualize VEGF in angiodysplasia lesions. HUVEC were incubated under hypoxic conditions or in the presence of bFGF. Effects of exposure to thalidomide were studied. Cell growth was assessed in methylthiazolyte‐trazolium assays. Enzyme‐linked immunosorbent assays and real‐time polymerase chain reaction were performed to assess the expression of VEGF at protein and mRNA levels. Western blot was performed to detect the expression of HIF‐1α under hypoxic conditions. Results: VEGF was strongly expressed in 75% of patients with angiodysplasia lesions, as compared to expression in patients without angiodysplasia lesions. VEGF was also induced in HUVEC under hypoxic conditions (P < 0.05). bFGF was found to stimulate the proliferation of HUVEC and enhance the expression of VEGF. Thalidomide suppressed bFGF‐induced proliferation significantly and decreased VEGF expression, both at the protein and mRNA levels. Thalidomide also inhibited HIF‐1α in a dose‐dependent manner (P < 0.05). Conclusions: VEGF may play an important role in the pathogenesis of angiodysplasia. Thalidomide can suppress VEGF, either induced by HIF‐1α or bFGF.     

弥漫大B细胞淋巴瘤患者血清血管内皮生长因子、碱性成纤维细胞生长因子水平检测分析

目的 探讨弥漫大B细胞淋巴瘤(DLBCL)患者血清血管内皮生长因子(VEGF)、碱性成纤维细胞生长因子(bFGF)的水平及临床意义.方法 选取2019年2月至2020年2月我院收治的DLBCL患者140例及同期在我院进行体检的健康者70例为研究对象.采用环磷酰胺+阿霉素+长春新碱+泼尼松(CHOP)方案对患者进行化疗....     

血管内皮生长因子在肺动脉平滑肌细胞重构中的作用

目的 :探讨血管内皮生长因子 （VEGF）在野百合碱 （MCT）性肺动脉高压 （PH）中的作用。方法 :用 MCT复制大鼠慢性 PH病理模型 ,用免疫组化法和图像分析技术测定肺组织中 VEGF的表达。结果 :发现 VEGF可在正常大鼠肺血管平滑肌、支气管平滑肌和软骨组织中表达 ,并且 MCT组 VEGF表达的相对含量在肺血管平滑肌 （177±7）和支气管平滑肌 （172± 6）均较正常组 （血管平滑肌 13 6± 8,支气管平滑肌 13 8± 12 ）呈显著增强 （P<0 .0 5）。结论 :MCT性 PH中 VEGF在肺血管平滑肌的过度表达参与 MCT性 PH的发病过程     

血管内皮生长因子及血管内皮生长因子受体在急性肺损伤中作用的研究

血管内皮生长因子是作用于血管内皮细胞的重要血管调节因子,它通过与内皮上的特异受体结合,可发挥促进内皮细胞增殖、分化、诱导血管生成、增加微血管通透性等多种功能.近年研究显示血管内皮生长因子在不同原因、不同阶段急性肺损伤中所起的作用不同.     

血管内皮生长因子基因转染骨髓间充质干细胞移植促进缺血心肌血管生成的研究

目的研究血管内皮生长因子(vascularendothelial growth factor,VEGF)基因转染骨髓间充质干细胞(mesenchymalstem cells,MSCs)移植对缺血心肌的血管生成作用。方法于2004年5月至2005年8月取第四军医大学西京医院分离、培养Wistar大鼠的MSCs,用真核表达载体pcDNA3.1(-)/hVEGF165转染MSCs。45只近交系Wistar大鼠随机均分为转染组(MSCs/VEGF组)、对照组(MSCs组)、无血清培养基组(DMEM组),结扎前降支建立急性心肌梗死模型后在梗死区边缘区行5×106细胞移植,DMEM组行等量培养基注射。细胞移植前行CM-DiI标记。移植1个月后行心脏B超测量射血分数值,组织化学染色评价新生血管密度。结果培养的MSCs呈典型贴壁生长成纤维样外观,pcDNA3.1(-)/hVEGF165能有效转染大鼠MSCs,移植1个月后MSCs/VEGF组较其余各组左室射血分数(LVEF),再生血管密度明显增加,差异均有显著性(P<0.01)。结论VEGF基因转染MSCs移植能显著促进缺血心肌血管再生,进而改善心脏功能。     

VEGF与VEGF-C蛋白在胆管癌中的表达及意义

目的探讨VEGF与VEGF-C蛋白在胆管癌的表达及其与临床病理特征的关系。方法采用免疫组化SP法检测49例胆管癌组织中vEGF与VEGF-C叠白的表达。结果胆管癌VEGF和VEGF—C蛋白的表达率分别为65．3％和69．4％。VEGF和VEGF-C蛋白的高表达与胆管癌淋巴结转移及分化程度有关。VEGF与VEGF—C的表达有显著相关性（P＜0．01）。结论VEGF和VEGF—C蛋白的表达与胆管癌侵袭转移有关。     

血管内皮细胞生长因子对肾小球内皮细胞通透性的影响

目的 :观察血管内皮细胞生长因子 (VEGF)对肾小球内皮细胞通透性的影响 ,并与脐静脉内皮细胞进行比较分析。　 方法 :采用二室弥散系统检测内皮细胞通透性。肾小球内皮细胞 (MGEC)和人脐静脉内皮细胞(HUVEC)接种于细胞培养嵌套的微孔滤膜 (孔径 0 4 5 μm)上 ,待细胞生长融合后 ,加入不同浓度的VEGF作为处理因素 ,以生物素标记的牛血清白蛋白 (biotin BSA)作为通透性指示剂 ,采用ELISA方法检测不同时间段biotin BSA通过细胞单层的百分数。　 结果 :正常培养条件下 ,生长在滤膜上的MGEC和HUVEC单层的通透性没有明显差异。VEGF可显著增加MGEC和HUVEC的通透性 ,呈剂量和时间依赖性。 1μg/LVEGF作用 12h可使MGEC对白蛋白的通透率增加近 2 5 % (0 31± 0 0 3vs 0 2 5± 0 0 3) ;VEGF浓度达 10 μg/L始显著增加HUVEC通透性 (0 2 8± 0 0 7vs0 2 1± 0 0 4 ) ,且远小于MGEC通透性增加的幅度 (P <0 0 1) ;VEGF浓度达 5 0 μg/L时 ,其增加内皮细胞通透性的作用基本达到饱和。 5 0 μg/LVEGF作用 0 5h即可使MGEC和HUVEC的蛋白通透率分别增加 10 0 % (0 12± 0 0 2vs0 0 6± 0 0 1)和 6 0 % (0 0 8± 0 0 3vs0 0 5± 0 0 1) ,并至少持续到 12h。　 结论 :首次在体外直接证实了VEGF具有增加MGEC