丁咯地尔对大鼠坐骨神经损害的保护作用

目的观察丁咯地尔对坐骨神经损害后恢复的影响。方法SD大鼠100只随机分为正常组、模型组、甲钴胺组(阳性对照组,104μg·kg~(-1))、丁咯地尔组(40 mg·kg~(-1))。以大鼠坐骨神经挤压伤建立动物模型,以坐骨神经传导速度、坐骨神经干病理切片(光镜、电镜)为观察指标,考察丁咯地尔对坐骨神经损害后恢复的影响。结果wk 4时甲钴胺组和丁咯地尔组均能显著增加坐骨神经传导速度,甲钴胺组与模型组比较有显著差异(P<0.05),丁咯地尔组与模型组比较有非常显著差异(P<0.01);4 wk时丁咯地尔组和甲钴胺组髓鞘形态结构接近正常,而模型组神经髓鞘溃变程度很高。结论丁咯地尔对坐骨神经损害有确切的修复作用。     

神经生长因子对大鼠坐骨神经损伤的修复作用

目的：观察大鼠坐骨神经横断挫伤后,外源性神经生长因子（NGF）对大鼠周围神经损伤的修复作用。方法：采用大鼠坐骨神经横断致伤方法,实验分为：假手术组、生理盐水对照组、NGF组,每组10只,观察时间为2wk。结果：术后2wk,NGF组的体感诱发电位（SEP）、运动诱发电位（MEP）与生理盐水对照组相比,潜伏期明显缩短（P＜0．05）。经Tarlov评分,NGF组有70％可恢复到4－5分,而生理盐水对照组只有20％恢复到4－5分。结论：NGF对周围神经损伤后有促进神经传导和损伤修复的作用。     

碱性成纤维细胞生长因子上调原代培养鼠星形胶质细胞中血管内皮生长因子的表达(英文)

目的:观察碱性成纤维细胞生长因子(bFGF)对鼠星形胶质细胞中血管内皮生长因子(VEGF)表达的影响。方法:用半定量聚合酶链反应(PCR)法和免疫组织化学法分别考察bFGF对VEGF信使RNA(mRNA)水平和蛋白质水平的影响。对不同剂量bFGF(1,10,100 ug·L~(-1))和不同孵育时间(3,6,12,24 h)的作用均进行了分析。 结果:bFGF可以剂量依赖性升高VEGF的mRNA水平。bFGF 10ug·L~(-1)在孵育3 h后即可上调VEGF mRNA水平,孵育24 h后细胞内VEGF mRNA水平显著高于对照组。免疫细胞化学分析结果表明bFGF也能升高细胞的VEGF蛋白质水平。结论:碱性成纤维细胞生长因子可以上调鼠星形胶质细胞中血管内皮生长因子的表达。     

Celecoxib,a selective cyclooxygenase-2 inhibitor,inhibits retinal vascular endothelial growth factor expression and vascular leakage in a streptozotocin-induced diabetic rat model

Overexpression of vascular endothelial growth factor (VEGF) is implicated in the development of vascular leakage and retinal neovascularization in diabetic subjects. The objective of this study was to determine whether celecoxib, a selective cyclooxygenase-2 enzyme inhibitor, reaches ocular tissues following oral administration and inhibits the retinal VEGF expression and vascular leakage in a streptozotocin-induced diabetic rat model. After administering a single intraperitoneal injection of streptozotocin (60 mg/kg) to Sprague-Dawley rats and ensuring the induction of diabetes at the end of 24 h, celecoxib was administered b.i.d. by oral gavage (50 mg/kg). On day 8, the animals were sacrificed and the retinal VEGF and cyclooxygenase-2 mRNA levels, ocular tissue celecoxib concentrations, and the vitreous/plasma protein ratio were determined. In diabetic rats, the retinal VEGF mRNA expression was 2.3-fold compared to controls, with a corresponding increase in cyclooxygenase-2 mRNA expression. Celecoxib treatment inhibited VEGF mRNA expression without any significant reduction in cyclooxygenase-2 mRNA. Furthermore, the retinal vascular leakage estimated as vitreous to plasma protein ratio increased in diabetic animals from 0.35+/-0.1 to 1.1+/-0.1 and celecoxib treatment significantly decreased this ratio to 0.4+/-0.1. Celecoxib levels were 24.8+/-6.6, 1.9+/-1, 1.7+/-0.8, and 6.9+/-0.9 ng/mg in the retina, vitreous, lens, and cornea, respectively. The plasma celecoxib levels were 85+/-24 ng/ml. Thus, celecoxib reaches the retina after oral administration and reduces diabetes-induced retinal VEGF mRNA expression and vascular leakage by inhibiting the activity of cyclooxygenase-2 enzyme.     

依达拉奉对大鼠坐骨神经损伤后脊髓脂质过氧化的影响

目的:探讨自由基清除剂依达拉奉对坐骨神经损伤后神经功能及脊髓脂质过氧化反应的影响.方法:Wistar大鼠48只,随机分为3组:坐骨神经挤压伤组、依达拉奉治疗组、假手术组.分别于7、14、21、28 d检测各组大鼠坐骨神经功能指数(SFI)、脊髓内过氧化物歧化酶(SOD)和丙二醛(MDA)的变化.结果:伤后各组大鼠SFI均降低,挤压伤组大鼠SFI较依达拉奉治疗组低(P<0.05),神经功能恢复较治疗组缓慢.伤后挤压伤组大鼠脊髓内SOD活性升高,依达拉奉治疗组大鼠脊髓内SOD活性与假手术组相比升高不明显(P>0.05).伤后挤压伤组大鼠脊髓内MDA含量上升明显,依达拉奉治疗组大鼠脊髓内MDA含量在各个时间点均显著低于挤压伤组大鼠脊髓内MDA含量(P相似文献   

血管内皮生长因子在乳腺癌中的表达及意义

目的：探讨血管内皮生长因子（VEGF）在乳腺癌中的表达及其临床意义。方法：应用免疫组织化学法检测74例乳腺癌组织中VEGF的表达。分析其与乳腺癌临床病理特征及预后的关系。结果：VEGF的阳性表达率为64．9％。VEGF的表达与肿瘤大小（P〈0．05）、临床分期（P〈0．05）、腋淋巴结转移（P〈0．05）有关。VEGF表达阴性和阳性两组5年总生存率（overall survival，OS）和无瘤生存率（disease free survival，DFS）差异有显著性（P〈0．05）。结论：VEGF阳性表达提示乳腺癌预后不良。VEGF可为判断乳腺癌预后的有效指标。     

血管内皮生长因子在乳腺癌中的表达及意义

目的研究血管内皮生长因子(VEGF)在乳腺癌中的表达情况及其与乳腺癌预后的关系,探讨其在乳腺癌中的预后价值。方法应用免疫组织化学法检测64例乳腺癌组织VEGF。结果VEGF的阳性表达率为63%。VEGF与肿瘤的大小、TNM分期、组织学分级、腋淋巴结转移呈正相关。结论VEGF为判断乳腺癌预后的有效指标。     

白果内酯刺激大鼠星形胶质细胞GDNF和VEGF表达(英文)

目的:观察白果内酯对大鼠星形胶质细胞GDNF和VEGF表达的影响。方法:应用半定量PCR了解大鼠星形胶质细胞分别经不同浓度白果内酯(0,5,15,50,100μmol·L~(-1))作用12、24和48h后细胞内GDNF和VEGF mRNA的变化,同时应用免疫组化了解经50μmol·L~(-1)作用24h后细胞内GDNF和VEGF蛋白的变化。结果:大鼠星形胶质细胞经50μmol·L~(-1)白果内酯作用12h后,细胞内GDNF和VEGF mRNA水平开始显著增高,经50μmol·L~(-1)作用24h后细胞胞浆内可见明显的VEGF和GDNF蛋白表达。结论:白果内酯可能通过诱导星形胶质细胞GDNF和VEGF的表达对神经细胞起保护作用。     

雷公藤内酯抑制内皮细胞血管内皮生长因子表达与合成

目的:研究雷公藤内酯对血管内皮细胞生长因子(VEGF)mRNA表达及VEGF合成与分泌的影响,进一步探讨雷公藤内酯降低肾小球肾炎患者尿蛋白的作用机制。方法:以人内皮细胞系ECV-304为研究对象,利用半定量逆转录聚合酶链反应(RT-PCR),流式细胞仪,酶联免疫吸附法(ELISA)检测不同剂量雷公藤内酯对佛波脂(TPA)诱导的内皮细胞VEGFmRNA表达及VEGF合成与分泌的影响,用RT-PCR检测雷公藤内酯对内皮细胞c-fos/c-jun mRNA表达的影响。结果:TPA能够明显上调VEGF mRNA表达,蛋白合成与分泌。而雷公藤内酯可以抑制TPA诱导的内皮细胞VEGF mRNA表达及VEGF蛋白合成与分泌,该作用在10μg·L~(-1)时更为明显。同样,雷公藤内酯剂量依赖性地抑制TPA诱导的内皮细胞c-fos/c-jun mRNA的表达。结论:雷公藤内酯通过影响c-fos/c-jun基因转录而抑制内皮细胞VEGFmRNA表达及VEGF合成与分泌是雷公藤内酯降低肾小球肾炎患者尿蛋白的作用机制之一。     

Targeted delivery of vascular endothelial growth factor improves stem cell therapy in a rat myocardial infarction model

Rebuilding of infarcted myocardium by mesenchymal stem cells (MSCs) has not been successful because of poor cell survival due in part to insufficient blood supply after myocardial infarction (MI). We hypothesize that targeted delivery of vascular endothelial growth factor (VEGF) to MI can help regenerate vasculature in support of MSC therapy in a rat model of MI. VEGF-encapsulated immunoliposomes targeting overexpressed P-selectin in MI tissue were infused by tail vein immediately after MI. One week later, MSCs were injected intramyocardially. The cardiac function loss was moderated slightly by targeted delivery of VEGF or MSC treatment. Targeted VEGF + MSC combination treatment showed highest attenuation in cardiac function loss. The combination treatment also increased blood vessel density (80%) and decreased collagen content in post-MI tissue (33%). Engraftment of MSCs in the combination treatment group was significantly increased and the engrafted cells contributed to the restoration of blood vessels.From the Clinical EditorVEGF immunoliposomes targeting myocardial infarction tissue resulted in significantly higher attenuation of cardiac function loss when used in combination with mesenchymal stem cells. MSCs were previously found to have poor ability to restore cardiac tissue, likely as a result of poor blood supply in the affected areas. This new method counterbalances that weakness by the known effects of VEGF, as demonstrated in a rat model.     

Cyclosporine A up-regulates expression of matrix metalloproteinase 2 and vascular endothelial growth factor in rat heart

Cyclosporine A (CsA) is the first immunosuppressant universally used in allotransplantation. However, it has been demonstrated that this drug produces side effects in several organs, particularly in the kidney and in the heart. Since the immunosuppressive therapy induces myocardial toxicity, the aim of this study was to evaluate in the myocardium of CsA-treated rats the expression variations of vascular endothelial growth factor (VEGF) and matrix metalloproteinase 2 (MMP2), to verify if: VEGF increased, VEGF increase was associated with MMP2 increase and they could be considered as repair proteins. The study was carried out on 28 Wistar rats divided into two groups. The group I animals served as control and so they were subcutaneously injected daily with castor oil for 21 days; group II: animals were subcutaneously injected daily with CsA (Sandimmun, Sandoz) at the therapeutic dose (15 mg/kg) for 21 days. The group I animals (control) showed normal heart architecture and low levels of MMP2 and VEGF. The group II animals (CsA-treated) showed structural degenerative changes with myocardial fibrosis and a clear increase both in MMP2 and VEGF. These data show that the immunosuppressant therapy induces a high increase in both the proteins and that VEGF variations are associated with MMP2 variations. These findings suggest that these proteins are involved in the endogenous emergency cell mechanisms induced by stress conditions, probably playing a role against myocardial injury as repair proteins.     

医用三氧对慢性坐骨神经损伤大鼠神经生长因子水平的影响

目的 探讨不同浓度医用三氧(O3)对慢性坐骨神经损伤(chronic constriction injury,CCI)大鼠神经生长因子水平的影响,为临床治疗神经病理性疼痛提供基础科学依据.方法 60只SPF级健康成年雄性SD大鼠随机分为假手术组、CCI组和不同浓度O3(15、30和60μg/ml依序为O3-15组、O3...     

宫颈癌微血管计数和血管内皮生长因子的表达

目的探讨微血管密度(MVD)和血管内皮生长因子(VEGF)表达与宫颈癌的临床病理联系及其相互关系。方法应用免疫组织化学方法检测和分析72例宫颈癌、24例正常宫颈组织中MVD和VEGF的表达情况。结果宫颈癌患者的微血管密度明显高于正常组织(P<0.01);宫颈浸润癌明显高于原位癌(P<0.01),浸润癌Ⅰ期与Ⅱ期差异无显著性(P>0.05);MVD随着病理分级增高呈递增趋势,组织学分级Ⅰ级与Ⅱ级、Ⅲ级差异有显著性(P<0.05);MVD增高与患者的生存期有关,生存期<5年者MVD明显高于生存期>5年者(P<0.05);MVD与临床分型、淋巴结转移无明显相关性(P>0.05)。VEGF在宫颈原位癌呈低表达,原位癌强阳性率明显低于浸润癌(P<0.05);VEGF表达强弱与病理组织学分级有关,分化程度低,恶性程度高,VEGF表达增强。VEGF表达阳性组的宫颈癌标本中MVD明显高于VEGF表达阴性组(P<0.05),且随着VEGF表达的增强,微血管密度随之增加,两者呈正相关。结论VEGF与宫颈癌的血管生成密切相关;MVD和VEGF表达与宫颈癌的恶性程度密切相关。     

Vasoactive factors and diabetic retinopathy: vascular endothelial growth factor, cycoloxygenase-2 and nitric oxide

The pathogenetic agents involved in the development of diabetic retinopathy are diverse. In the setting of hyperglycaemia and retinal hypoxia a number of vasoactive factors may interact to promote pathology in a variety of cell types including the microvasculature, neurons and glia. Vascular endothelial growth factor (VEGF) is universally accepted as a primary factor in the regulation of vessel patency in vascular networks throughout the body and including the retina. There is considerable evidence that the VEGF system in disturbed early in diabetes and interacts with other pathways and vasoactive factors to stimulate breakdown of the blood retinal barrier (BRB) and eventually promote angiogenesis, the hallmark feature of proliferative diabetic retinopathy (PDR). There is a distinct relationship between VEGF and the prostaglandin-cyclooxygenase system. Prostaglandins influence retinal blood flow, are important in inflammation and are also pro-angiogenic. Recent evidence suggests that cyclooxygenase-2 (COX-2) modulates angiogenesis by interacting with the VEGF system. Like prostaglandins, nitric oxide (NO) is a vasodilator and is implicated in VEGF mediated vascular permeability and angiogenesis. Emerging evidence indicates that COX-2 also interacts with NO and that these two systems have reciprocal effects on each other. There is little doubt that the interactions between these three vasoactive systems are complex and requires further study in the context of retinal vascular permeability, angiogenesis and neurodegeneration. This review will explore experimental and clinical evidence that VEGF, COX-2 and NO promote retinal pathology in diabetes and other ischemic-induced retinopathies.     

Inhibition of vascular endothelial growth factor expression and production by triptolide

Triptolide, the major component of the diterpenoids of the Chinese herb Tripterygium wilfordii Hook f. (Celastraceae), inhibited vascular endothelial growth factor expression and secretion in endothelial cells treated by 12-O-tetradecanoylphorbol 13-acetate dose-dependently. This effect may be one of the mechanisms underlying the therapeutic effects of triptolide on rheumatoid arthritis.     

Effect of vascular endothelial growth factor C (VEGF-C) gene transfer in rat model of secondary lymphedema

Secondary lymphedema has been clinically well described, but a cure is still lacking. Although there have been previous investigations using plasmid DNA for gene therapy, few have focused on the use for the treatment of lymphedema. Therefore, we investigated the effects of VEGF-C gene transfer for the treatment of lymphedema using our plasmid pcDNA3.1-VEGF-C. We produced a surgical model of secondary lymphedema in the rat hindlimb and treated with local intradermal VEGF-C transfection to investigate the efficacy of gene transfer. Magnetic resonance imaging (MRI) (P<0.05), B ultrasound (P<0.05), and water displacement volumetry (P<0.05) demonstrated a reduction of lymphedema in therapy group as compared to controls. Histological and immunofluorescent studies demonstrated numerous newly formed lymphatic vessels in therapy group. Our results indicate that VEGF-C gene therapy has produced new lymphatic vessels which may have improved functional lymphatic drainage to reduce lymphedema volume in our model.     

Effect of vascular endothelial growth factor C (VEGF-C) gene transfer in rat model of secondary lymphedema

Secondary lymphedema has been clinically well described, but a cure is still lacking. Although there have been previous investigations using plasmid DNA for gene therapy, few have focused on the use for the treatment of lymphedema. Therefore, we investigated the effects of VEGF-C gene transfer for the treatment of lymphedema using our plasmid pcDNA3.1-VEGF-C. We produced a surgical model of secondary lymphedema in the rat hindlimb and treated with local intradermal VEGF-C transfection to investigate the efficacy of gene transfer. Magnetic resonance imaging (MRI) (P<0.05), B ultrasound (P<0.05), and water displacement volumetry (P<0.05) demonstrated a reduction of lymphedema in therapy group as compared to controls. Histological and immunofluorescent studies demonstrated numerous newly formed lymphatic vessels in therapy group. Our results indicate that VEGF-C gene therapy has produced new lymphatic vessels which may have improved functional lymphatic drainage to reduce lymphedema volume in our model.     

转化生长因子β1和VEGF在甲状腺癌组织中的表达及其与血管生成的关系

目的探讨转化生长因子(TGF)β1和血管内皮生长因子(VEGF)在甲状腺癌组织中的表达及其与肿瘤血管生成的关系.方法采用免疫组织化学方法,检测46例甲状腺癌组织中TGFβ1与VEGF表达及肿瘤微血管计数(MVC).结果 46例甲状腺癌组织中TGFβ1阳性表达率为63.04%(29/46),TGFβ1阳性表达者MVC值(26.18±4.05)显著大于阴性表达者(20.13±4.29),VEGF阳性表达者35例,阳性表达率为79.06%,VEGF阳性表达者MVC值(25.82±3.61)亦显著大于阴性表达者(19.65±6.32)(均P＜0.05),TGFβ1、VEGF阳性表达率在乳头状癌、滤泡癌、髓样癌及未分化癌中两两比较差异均无统计学意义(P＞0.05),在Ⅰ、Ⅱ、Ⅲ、Ⅳ期甲状腺癌中两两比较差异也均无统计学意义(P＞0.05).结论 TGFβ1与VEGF表达与甲状腺癌组织学分型、临床分期无关,但参与甲状腺癌肿瘤血管生成过程.