外源性碱性成纤维细胞生长因子对血管性痴呆患者血管内皮生长因子的影响

目的 研究外源性碱性成纤维细胞生长因子对血管性痴呆患者用药前后血清血管内皮生长因子的影响。方法 选择血管性痴呆患者60例、采用临床痴呆评定量表(CDR)筛选出轻度血管性痴呆患者60例,分成轻度痴呆治疗组34例,轻度痴呆对照组26例,正常对照组30例,通过给予患者外源性碱性成纤维细胞生长因子氧气雾化吸入,分别对各组患者治疗前、治疗后14d、30d及正常对照组血清血管内皮生长因子的观察。结果 两组患者治疗前血清血管内皮生长因子明显低于正常对照组,痴呆治疗组患者治疗后14d、30d 血清血管内皮生长因子逐渐升高,与痴呆对照组相比有统计学意义(P<0.001)。结论 外源性碱性成纤维细胞生长因子通过鼻黏膜进入中枢神经系统,促进血清血管内皮生长因子的生成,从而表明bFGF可能可诱导脑内神经元发生,达到治疗目的。     

血管性痴呆患者血清miR-17和VEGF表达及相关性

目的检测血管性痴呆(VD)患者血清中miR-17和血管内皮生长因子(VEGF)的表达情况,探讨二者的表达关系及临床意义。方法选取87例VD患者作为观察组,其中轻度组25例,中度组39例,重度组23例,同期选取体检的健康者65例作为对照组。采用简易智能状态检测(MMSE)量表对受试者进行评分;采用实时荧光PCR(qRT-PCR)法检测血清中miR-17表达水平;采用酶联免疫吸附试验(ELISA)检测血清中VEGF水平;分析miR-17和VEGF在VD患者血清中表达的相关性。结果观察组MMSE评分显著低于对照组(P<0.05)。与对照组比较,VD患者血清miR-17和VEGF表达水平均显著下调(P<0.05)。重度组患者血清miR-17和VEGF表达水平均显著低于中度组和轻度组(P<0.05),中度组患者血清miR-17和VEGF水平均显著低于轻度组(P<0.05)。血清miR-17和VEGF水平均与VD患者MMSE评分呈正相关(P<0.05)。VD患者血清中miR-17与VEGF水平表达呈正相关(P<0.05)。结论miR-17和VEGF在VD患者血清中明显低表达,二者可能与VD疾病的发生和病情发展有关。     

卡托普利对兔动脉粥样硬化斑块内碱性成纤维细胞生长因子和血管内皮生长因子的影响

目的　观察碱性成纤维细胞生长因子 (b FGF)和血管内皮生长因子 (VEGF)与动脉粥样硬化 (AS)的关系 ,以及卡托普利 (captopril)对 AS和 b FGF、VEGF表达的影响。方法　 36只兔随机分为 3组 :空白对照组 ( 组 )动物喂饲普通颗粒饲料 ;实验对照组 ( 组 )动物喂饲含 1g/d胆固醇和 3%猪油的饲料 ;实验组 ( 组 )喂饲含 1g/d胆固醇和 3%猪油的饲料 ,同时给予卡托普利 10 mg.kg- 1 .d- 1 。于 12周后处死动物 ,取出主动脉做 b FGF和 VEGF免疫组化定性和定量观察。结果　光镜下 组和 组有明显 AS形成。定量研究 :与 I组相比 , 组和 组 b FGF在主动脉内中膜的表达面积 (μm2 ) (2 6 999.6 8± 9931.82 ,2 4 0 75 .6 2± 2 4 787.6 8对 1386 8.14± 3180 .13)、密度 (5 .4 3±1.6 5 ,3.33± 1.15对 2 .0 7± 0 .78)和密度指数 (15 7886 .4 6± 113340 .0 5 ,73348.6 0± 4 6 0 4 8.81对 2 92 90 .78±15 0 16 .5 8)均有非常显著性增加 (P<0 .0 1) ,但 组与 组相比 ,其 b FGF表达的面积、密度和密度指数均有非常显著性降低 (P<0 .0 1)。与 组相比 , 组和 组 VEGF在主动脉内中膜的表达面积 (30 4 2 5 .4 3± 11114 .14 ,2 55 2 9.31± 10 30 5 .88对 1386 8.14± 3180 .13)、密度 (6 .10± 2 .0 9,6 .10± 2 .     

复方苦参注射液联合化疗治疗对结直肠癌患者血清血管内皮生长因子的影响

目的评价复方苦参注射液联合化疗治疗结直肠癌的临床疗效及对血清血管内皮生长因子(VEGF)表达的影响。方法抽取该院诊治的90例确诊为结直肠癌的患者,随机分为两组。观察组45例予复方苦参注射联合化疗;对照组45例予单纯化疗。观察两组患者临床疗效及不良反应,并采用酶联免疫吸附法(ELISA)检测患者血清VEGF水平。结果观察组有效率(82.22%)高于对照组(44.44%)(P<0.01);观察组不良反应发生率(8.89%)低于对照组(28.89%)(P<0.01)。治疗后5、30 d两组结直肠癌患者的血清VEGF水平均低于治疗前(P<0.01)。治疗后5 d,观察组结直肠癌患者的血清VEGF水平(192.8±30.4)pg/ml低于对照组(294.7±35.1)pg/ml(P<0.01)。治疗后30 d,观察组结直肠癌患者的血清VEGF水平(173.2±31.7)pg/ml低于对照组(267.8±34.2)pg/ml(P<0.01)。结论复方苦参注射液联合化疗治疗结直肠癌的疗效显著,可以有效提高患者生活质量,减少不良反应发生率,并能有效改善结直肠癌患者的血清VEGF水平。     

大肠癌患者垂体肿瘤转化基因、碱性成纤维细胞生长因子及血管内皮生长因子-C水平检测意义

目的通过检测大肠癌患者体内垂体肿瘤转化基因(PTTG)、碱性成纤维细胞生长因子(b FGF)及血管内皮生长因子(VEGF)-C的表达水平,探讨其在大肠癌发生发展过程中的作用及相互间关系。方法接受手术治疗的大肠癌(肿瘤组)患者78例的大肠腺癌组织标本。另外收集经病理证实是正常黏膜的组织标本18例作为正常组。比较两组PTTG、b FGF以及VEGF-C的阳性表达率以及上述三种因子各自与大肠癌临床病理分期的关系。结果肿瘤组PTTG、b FGF以及VEGF-C阳性细胞表达率均明显比正常组高(P0.01)。PTTG、b FGF以及VEGF-C表达在不同的分化程度、性别以及年龄的组别差异无统计学意义(P0.05);而在浸润深度、淋巴结转移情况以及Dukes分期比较均有统计学差异P0.05)。结论PTTG、b FGF和VEGF-C在老年大肠癌的发生和发展过程中发挥着重要的作用,其中促淋巴管以及血管生成的作用在大肠癌发生、发展以及转移、侵袭中均起了重要的作用,已是治疗肿瘤的一个新靶点。     

肝细胞生长因子与冠状动脉狭窄程度的相关性研究

目的:探讨肝细胞生长因子(HGF)、血管内皮生长因子(VEGF)、肿瘤坏死因子-α(TNF-α)与冠心病病变程度的相关性。方法:63例冠心病患者根据冠状动脉狭窄程度分为3组:轻度组18例,中度组22例,重度组23例,采用酶联免疫吸附法检测外周血HGF、VEGF、TNF-α水平,与20例年龄和性别相当的健康者(对照组)进行比较。冠心病患者按心绞痛分级Ⅰ级12例,Ⅱ级14例,Ⅲ级15例,Ⅳ级22例,与HGF、VEGF、TNF-α水平进行相关分析。结果:血清HGF水平重度组、中度组及轻度组明显高于对照组,有极显著性差异(P<0.01);血清VEGF、TNF-α水平重度组、中度组均明显高于轻度组及对照组,有极显著性差异(P<0.01);HGF、VEGF、TNF-α水平与心绞痛分级呈正相关(r1=0.864P<0.01;r2=0.682P<0.01;r3=0.403P<0.01)。结论:HGF、VEGF、TNF-α与心绞痛程度呈显著正相关,其中HGF较其他两项指标相关性更好。     

沙利度胺联合GP方案治疗晚期非小细胞肺癌的疗效及对血清VEGF、bFGF、TNF-α和生活质量的影响

目的探讨沙利度胺(TGP)联合顺铂和吉西他滨(GP)方案治疗晚期非小细胞肺癌(NSCLC)的疗效及对血清血管内皮生长因子(VEGF)、碱性成纤维细胞生长因子(b FGF)和肿瘤坏死因子(TNF)-α及生活质量的影响。方法选择晚期NSCLC患者80例,按照乱数表法分为研究组和对照组均40例。对照组采用GP治疗方案,研究组在对照组的基础上联用TGP治疗,两组均治疗42 d。两组分别于治疗前、治疗后测定血清VEGF、b FGF和TNF-α水平,并应用欧洲癌症研究与治疗组织(EORTC)生活质量量表(QLQ-C30)评定患者的生活质量。结果两组有效率无显著差异(P>0.05)。治疗后研究组血清VEGF、b FGF和TNF-α水平较治疗前显著降低,且显著低于对照组(P<0.05),对照组无明显变化(P>0.05)。治疗后,两组恶心呕吐、食欲、便秘评分较治疗前显著升高,气促评分较治疗前显著降低(P<0.05),对照组整体生活质量评分显著低于治疗前(P<0.05)。治疗后研究组整体生活质量、食欲、便秘评分显著高于对照组,恶心呕吐、气促评分显著低于对照组(P<0.05)。结论 TGP联合GP方案治疗晚期NSCLC的疗效与单独GP方案相当,但患者血清VEGF、b FGF和TNF-α水平下降更明显,生活质量得到更好的改善。     

银杏叶提取物片对轻中度血管性痴呆β-Ap、VEGF的影响

目的 观察银杏叶提取物片对血管性痴呆(VD)病人血清β淀粉样蛋白(β-Ap)、血管内皮生长因子(VEGF)的影响.方法 将50例VD患者随机分为治疗组与对照组,每组各25例,比较治疗前后两组血清β-Ap、VEGF的含量变化,以及简易精神状态检查量表(MMSE)、日常生活能力量表(ADL)积分变化.结果 两组治疗后β-Ap含量较治疗前下降(P＜0.05),VEGF含量较治疗前升高(P＜0.05);但组间治疗后比较治疗组优于对照组(P＜0.05).治疗组治疗后MMSE评分明显升高,ADL评分明显降低,差异有统计学意义(P＜0.01).两组治疗后MMSE评分差异无统计学意义,但治疗前后差值有统计学意义(P＜0.05);两组治疗后ADL评分及治疗前后差值差异均有统计学意义(P＜0.05).结论 银杏叶提取物片能改善VD病人的认知功能,降低β-Ap含量,增加VEGF含量.从而减轻缺血缺氧性损害,改善脑血流,促进病人康复.     

皮质下动脉硬化性脑病患者P选择素和血管内皮生长因子的表达及相关性

目的通过对皮质下动脉硬化性脑病(SAE)患者P选择素和血管内皮生长因子(VEGF)表达的测定及相关性比较,探讨二者在SAE中的作用和意义。方法选择SAE患者83例(SAE组)和健康体检者57例(对照组),采用酶联免疫法测定2组空腹血浆P选择素和血清VEGF,同时检测空腹血糖、血脂、C反应蛋白(CRP),并进行相关性分析。结果与对照组比较,SAE组P选择素、VEGF表达水平明显升高,差异有统计学意义(P<0.01)。SAE组轻度痴呆患者P选择素和VEGF表达水平明显低于中、重度痴呆患者,而中、重度痴呆患者间差异无统计学意义。SAE组P选择素与血糖、TG、CRP呈正相关,与年龄、TC、HDL-C不相关;VEGF与TC、CRP呈正相关,与年龄、血糖、TG、HDL-C不相关;P选择素与VEGF呈正相关。结论SAE患者P选择素和VEGF水平明显升高,可能共同参与了SAE的血栓形成和组织修复过程,临床中给予抗血小板药物,对SAE的预防可能有重要意义。     

盐酸法舒地尔注射液对急性脑梗死患者血清血管内皮生长因子、血管生长素-1浓度的影响

目的观察盐酸法舒地尔注射液对急性脑梗死(ACI)患者血清血管内皮生长因子(VEGF)和血管生成素(Ang)-1浓度的影响。方法采用前瞻性随机、对照试验方案,连续选取82例住院治疗的ACI患者,分为治疗组44例,对照组38例。对照组采用控制血压、抗血小板聚集、调脂等常规治疗,治疗组在常规治疗基础上给予盐酸法舒地尔注射液30 mg加入0.9%生理盐水250 ml静脉滴注,每日2次,共治疗14 d。所有入选患者均于治疗前、治疗后第3天、第7天、第14天清晨取肘静脉血,采取双抗体夹心联酶免疫吸附(ELISA)法测定血清VEGF、Ang-1浓度。结果治疗后两组美国国立卫生研究院脑卒中量表(NIHSS)评分较治疗前均有明显改善,但治疗组NIHSS评分改善较对照组更为显著(P<0.01)。治疗第3天、第14天时治疗组与对照组比较VEGF变化无统计学差异(P>0.05),至第7天时两组比较有显著差异(P<0.01)。治疗后第3天、第7天时治疗组与对照组比较Ang-1变化无统计学意义(P>0.05),至第14天时两组比较有统计学差异(P<0.05)。治疗组、对照组在治疗后第7天、第14天与各组治疗前相比,VEGF变化有统计学意义(P<0.05),血清VEGF浓度在治疗后第7天达到高峰。治疗组、对照组在治疗后第14天分别与各组治疗前相比,Ang-1变化有统计学差异(P<0.05),血清Ang-1浓度在治疗后第14天仍呈上升趋势。结论法舒地尔可促进脑缺血后VEGF、Ang-1的高表达,促进血管新生,改善神经功能缺损。     

血管内皮生长因子及其受体在肺气肿患者肺组织中的表达

目的探讨血管内皮生长因子(VEGF)及其受体2(VEGF受体2/KDR)在肺气肿患者肺组织中的表达及其与肺气肿的相关性。方法取35例行肺叶切除术患者[A组(吸烟伴肺气肿组)16例,B组(不吸烟肺功能正常组)14例,C组(吸烟但肺功能正常组)5例]的外周肺组织标本,ELISA法检测肺组织匀浆中VEGF的含量,免疫组化法检测KDR蛋白表达,RT PCR检测VEGF和KDRmRNA水平,TUNEL法检测肺泡隔细胞的凋亡。结果A组患者肺组织VEGF、KDR表达均低于B组(P<0.01),肺泡隔细胞凋亡率高于B组(P<0.01)。C组与B组相比,VEGF及KDR表达差异无统计学意义(P>0.05)。结论VEGF及KDR水平减少与肺泡隔细胞凋亡的增加可能与肺气肿的发生相关。     

Novel vascular endothelial growth factor binding domains of fibronectin enhance vascular endothelial growth factor biological activity

Interactions between integrins and growth factor receptors play a critical role in the development and healing of the vasculature. This study mapped two binding domains on fibronectin (FN) that modulate the activity of the angiogenic factor, vascular endothelial growth factor (VEGF). Using solid-phase assays and surface plasmon resonance analysis, we identified two novel VEGF binding domains within the N- and C-terminus of the FN molecule. Native FN bound to VEGF enhanced endothelial cell migration and mitogen-activated protein (MAP) kinase activity, but FN that is devoid of the VEGF binding domains failed to do so. Coprecipitation studies confirmed a direct physical association between VEGF receptor-2 (Flk-1) and the FN integrin, alpha5beta1, which required intact FN because FN fragments lacking the VEGF binding domains failed to support receptor association. Thrombin-activated platelets released intact VEGF/FN complexes, which stimulated endothelial cell migration and could be inhibited by soluble high affinity VEGF receptor 1 and antibodies to alpha5beta1 integrin. This study demonstrates that FN is potentially a physiological cofactor for VEGF and provides insights into mechanisms by which growth factor receptors and integrins cooperate to influence cellular behavior.     

Hepatocyte growth factor and vascular endothelial growth factor in ischaemic heart disease

BACKGROUND: Hepatocyte growth factor (HGF) and vascular endothelial growth factor (VEGF) are endothelial cell-specific growth factors, but the production of these growth factors in cardiomyocytes has also been demonstrated. However, there have been no reports focusing their attention on the changes in these growth factors after coronary intervention. We investigated the time-course changes of the serum VEGF and HGF levels in angina pectoris (AP) and acute myocardial infarction (AMI). METHODS: The serum HGF and VEGF levels were measured in 60 patients with AP, in 62 patients with AMI (AP, before heparin administration, and at 24 and 48 hours, and one week after intervention; AMI, before heparin, and at 48 and 72 hours, and one, two, three and four weeks) and in 56 patients with neurocirculatory asthenia as controls. We defined the patients with remodelling who showed an increase in left ventricular end-diastolic volume index (LVEDVI) in the sub-acute phase of AMI. RESULTS: Hepatocyte growth factor levels in the AP and AMI were significantly higher than that in the control (p<0.0001). The AMI level was also significantly higher than AP (p<0.001). In the AMI and AP, HGF peaked at 48 hours. Vascular endothelial growth factor level in the AMI was significantly higher than that in the control and AP (p<0.0001). In the AMI, VEGF peaked at two weeks. There was a significant positive correlation between the peak VEGF and LVEDVI in the sub-acute phase of AMI (p=0.0089, r=0.436). Peak VEGF in the remodelling (+) group was significantly higher than that in the remodelling (-) group (p<0.001). In the AP, VEGF was unchanged. CONCLUSION: While both myocardial and vascular damage contribute to an increase in HGF level, vascular damage is not associated with the increase in VEGF. Vascular endothelial growth factor might be related to left ventricular remodelling in the sub-acute phase of myocardial infarction.     

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.     

神经发生、血管内皮生长因子与血管性认知损害

神经发生是神经前体细胞自我增殖和分化产生新神经元的动态过程。研究证实,海马神经发生可改善认知功能,并且血管内皮生长因子(vascular endothelial growth factor, VEGF)在神经发生中发挥着重要的调控作用。文章就 VEGF 促进神经发生的机制以及神经发生改善血管性认知损害的作用进行了综述。     

Vascular endothelial growth factor and vascular homeostasis

Vascular endothelial growth factor (VEGF) is the angiogenic factor promoting and orchestrating most, if not all, processes of neovascularization taking place in the embryo and the adult. VEGF is also required to sustain newly formed vessels and plays additional multiple roles in the maintenance and function of certain mature vascular beds. Correspondingly, perturbations in VEGF signaling may impact organ homeostasis in multiple ways. Here we briefly review potential consequences of VEGF loss of function in adult organs. Different vascular beds display highly variable dependencies on VEGF for survival, and its loss of function may trigger the regression of many VEGF-dependent vasculatures. Normal turnover of blood vessels, in conjunction with the fact that VEGF is indispensable for compensatory angiogenesis to restore adequate perfusion, accounts for progressive vascular rarefaction under conditions of chronic VEGF inhibition of even vasculatures that are not intrinsically dependent on VEGF. Because blood vessels may have paracrine functions other than their traditional role in tissue perfusion, vascular regression resulting from VEGF withdrawal may cause substantial collateral tissue damage. VEGF may also impact tissue homeostasis via acting directly on nonvascular cells expressing cognate receptors. In the particular case of the lung, constitutive abundant expression of VEGF together with the fact that its receptors are distributed on both endothelial and epithelial cells is compatible with multiple homeostatic VEGF functions in the adult lung. Indeed, experimental inhibition of VEGF in the mature lung produces lesions resembling common lung pathologies, including emphysema and respiratory distress syndrome.     

Therapeutic angiogenesis using vascular endothelial growth factor

Therapeutic angiogenesis using vascular endothelial growth factor can reduce tissue ischemia by simulating the natural process of angiogenesis. Vascular endothelial growth factor not only stimulates endothelial cells to proliferate and migrate, but also mobilizes endothelial progenitor cells and achieves vascular protection. Besides direct administration of angiogenic proteins, plasmids and viral vectors carrying angiogenic genes have been used. Animal experiments have shown promise with evidence of neovascularization and improved perfusion in the target myocardium. Initial phase I and II clinical trials results are encouraging and reflect the potential success of therapeutic angiogenesis as a clinical modality for the treatment of ischemic heart disease. This review discusses the role of vascular endothelial growth factor in therapeutic angiogenesis, along with the problems and considerations of this approach as a treatment strategy.     

Clinical significance of vascular endothelial growth factor and hepatocyte growth factor in multiple myeloma

Angiogenesis is a crucial process in the progression of multiple myeloma (MM). Vascular endothelial growth factor (VEGF) and hepatocyte growth factor (HGF) are multifunctional cytokines that potently stimulate angiogenesis including tumour neovascularization. Serum levels of VEGF and HGF were measured in 52 patients with MM by enzyme-linked immunosorbent assay (ELISA). Serum levels of VEGF and HGF were elevated in MM patients compared with healthy controls (VEGF: mean 0.31 ng/ml and 0.08 ng/ml respectively, P < 0.01; HGF: mean 2.17 ng/ml and 0.45 ng/ml, respectively, P < 0.001). In serial samples taken after chemotherapy, serum VEGF and HGF levels were correlated with M-protein levels. Serum levels of VEGF were higher in patients with extramedullary plasmacytomas than in patients without them (P < 0.05). They were also significantly higher in a group of patients who showed poor response to chemotherapy (P < 0.01). Serum levels of HGF were higher in patients with complications such as anaemia, hypercalcaemia and amyloidosis than in patients without these complications (P < 0.01, P < 0.05, P < 0.05 respectively). Both serum VEGF and HGF levels were significant predictors of mortality (P = 0.01, P = 0.02, respectively, log-rank test). The present study demonstrated that serum levels of VEGF and HGF are significantly elevated and dependent on the severity of MM, suggesting that measurement of VEGF and HGF may be useful for assessing disease progression and for predicting the response to chemotherapy in MM patients.