非那雄胺对大鼠前列腺增生组织血管内皮生长因子和微血管密度的影响

目的 探讨非那雄胺对大鼠前列腺增生组织血管内皮生长因子(VEGF)和微血管密度(MVD)的影响. 方法 雄性SD大鼠40只,隔日于颈部皮下注射丙酸睾丸酮(连续28 d),建立大鼠前列腺增生模型,之后将大鼠随机分为5组:A组灌胃给予安慰剂,B、C、D、E组灌胃给予非那雄胺,持续时间分别1周,2周,3周,4周.采用免疫组化法检测大鼠前列腺组织中VEGF和MVD的表达. 结果 A组前列腺组织中VEGF的表达和MVD明显高于B、C、D、E组,差异有统计学意义(P<0.05);B组前列腺组织中VEGF的表达和MVD高于D、E组,差异有统计学意义(P<0.05);C组前列腺组织VEGF的表达和MVD高于D、E组,差异有统计学意义(P<0.05);B组前列腺组织中VEGF的表达和MVD与C组比较差异无统计学意义(P>0.05);D组前列腺组织中VEGF的表达和MVD与E组之间比较差异无统计学意义(P>0.05). 结论 非那雄胺可以抑制大鼠前列腺组织中VEGF的表达,降低腺体内微血管密度,并且其抑制程度与非那雄胺的作用时间有关.     

戈舍瑞林对前列腺组织微血管密度及血管内皮生长因子影响的基础研究

目的：探讨戈舍瑞林对前列腺组织微血管密度（ MVD ）及血管内皮生长因子（ VEGF ）影响。方法：随机选取60只雄性SD大鼠,并且随机分成A、B、C、D、E、F六组;A组采取正常的饲养方式,其余各组均进行隔日颈部皮下注射丙酸睾丸酮建立大鼠前列腺增生模型,在第29天时随机选取一组（ B）处死观察模型是否建立成功,并取前列腺组织进行HE染色;剩余各组中,C组灌注生理盐水（15mL／kg）,D、E、F每日给予等量的戈舍瑞林溶液灌胃（1．0mg／kg）,分别持续1～3周后处死,观察各组前列腺增生例数、前列腺重量、VEGF 在前列腺组织中的表达、MVD在前列腺组织中的表达差异。结果：A、B、C、D、E、F六组大鼠中,A组正常饲养,结果大鼠前列腺没有发生增生,B、C、D、E、F五组均有不同程度的前列腺增生,并且每组10只老鼠全部发生增生。 B、C、D、E、F五组前列腺增生重量分别于A组比较,发现重量均明显高于A组,差异具有统计学意义（ P＜0．05）,五组之间采用单因素方差分析及组间比较差异不具有统计学意义（ P＞0．05）;C、D、E、F四组前列腺增生模型大鼠中,C组未采用戈舍瑞林灌胃,其VEGF阳性细胞面积、MVD均显著高于D、E、F三组,差异具有统计学意义（ P＜0．05）;D、E组间VEGF阳性细胞面积、MVD间差异不具有统计学意义（ P＞0．05）;D、E两组的VEGF阳性细胞面积、MVD均明显高于采用戈舍瑞林灌胃时间更长的F组,且差异具有统计学意义（ P＜0．05）。结论：前列腺增生模型大鼠的前列腺组织微血管密度（ MVD）及血管内皮生长因子（ VEGF）表达水平明显增高,戈舍瑞林能够有效降低MVD、VEGF的表达水平。     

VEGF、MVD与角膜新生血管形成关系的实验研究

目的 探讨血管内皮生长因子( vascular endothelial growth factor , VEGF )在大鼠角膜碱烧伤后新生血管形成中的作用.方法 利用氢氧化钠烧灼大鼠角膜表面,建立大鼠角膜新生血管(corneal neovascularization, CNV)模型,每日裂隙灯下观察角膜新生血管的发展,并分别于烧伤后1、4、7、14、21d处死大鼠,摘除角膜做病理切片,行微血管密度(Microvessel density,MVD)测定;免疫组化法检测VEGF的表达;图像分析系统测定该因子的蛋白表达.结果 免疫组化显示:VEGF在CNV中的阳性表达逐渐增加,于7 d表达最明显, 21 d后几乎无表达;MVD测定结果以CNV 7～14 d组血管密度最高;图像分析系统结果与免疫组化染色结果一致.结论 碱烧伤后CNV形成中,VEGF的表达增加,CNV中MVD与VEGF的表达呈正相关.     

非那雄胺对前列腺增生组织中微血管密度调控的机制探讨

目的 探讨非那雄胺对前列腺增生症组织中微血管调节因子表达的影响及意义.方法 取正常前列腺(NP)5例,前列腺增生症服用非那雄胺者(BPH+Finas)10例,前列腺增生症未服用非那雄胺者(BPH)30例的前列腺组织标本,采用免疫组化检测微血管调节因子内皮生长抑素(endostatin)、血管生长抑素(angiostatin)、血管形成因子-2(an-giopoietin-2)及血管内皮生长因子(VEGF)的表达,图像分析系统测量表达强弱.结果 BPH组endostatin、angiostatin表达较NP组明显减弱,而BPH+Finas组表达较BPH组明显增强;BPH组VEGF表达较NP组明显增强,而BPH+Finas组表达较BPH组明显减弱.endostatin阳性细胞计数(个/10Hp)在NP、BPH、BPH+Finas 3组分别为(129.00±10.68)、(34.00±15.38)、(142.10±12.22);angiostatin阳性细胞计数(个/10Hp)分别为(151.00±21.64)、(54.63±28.93)、(162.30±21.81);VEGF(灰度值)分别为(139.38±8.90)、(83.81±25.73)、(108.094-7.77),以上3组测值NP组和BPH+Finas组与BPH组比较差异均有显著性意义(均P<0.01).angiopoietin-2阳性细胞计数(个/10Hp)分别为(16.40±2.19)、(15.03±2.82)、(13.90±3.00),差异无显著性意义.结论 微血管调节因子endostatin、angiostatin、VEGF作用于局部组织的微循环,可能在前列腺增生症的病理生理过程中起重要调节作用.非那雄胺通过影响局部组织微血管调节因子,而发挥抑制前列腺增生的作用.     

胃癌中微血管密度及VEGF、NOS表达与肿瘤浸润、转移的相关性

目的:研究胃癌组织中微血管密度(MVD)的分布,血管内皮生长因子(VEGF),一氧化氮合酶(NOS)的表达及与肿瘤病理特征间的关系,探讨MVD、VEGF、NOS在胃癌浸润、转移中的意义及其间的相关性。方法:应用免疫组化SP法检测56例手术切除人胃癌组织石蜡包埋标本的VEGFi、NOS、eNOS、nNOS的蛋白表达,对肿瘤微血管以CD34抗体染色并检测MVD。结果:56例胃癌组织MVD值平均为36.25±6.32;VEGFi、NOS、eNOS、nNOS的阳性表达率分别为69.6%、75.0%、80.4%、83.9%;不同浸润深度、淋巴结转移程度及TNM分期的胃癌中MVD值的差异分别有统计学意义(P<0.01);VEGFi、NOS、eNOS、nNOS的表达随胃癌浸润深度的加深,淋巴结转移程度的提高而上调(分别为P<0.05,P<0.01,P<0.01,P<0.01);VEGFi、NOS阳性表达胃癌组织中的MVD值高于阴性表达者(分别为P<0.05,P<0.01);VEGF及iNOS表达均阳性者34例,VEGF表达阳性,iNOS表达阴性者5例,两者表达均阴性8例,iNOS的表达与VEGF表达有关(P<0.01)。结论:随着胃癌浸润,转移程度进展,肿瘤MVD值增高,VEGF、NOS的表达上调;胃癌中VEGF及iNOS的表达与肿瘤MVD有关,提示VEGF及iNOS在胃癌生长,浸润及转移中促进肿瘤新生血管形成;iNOS表达与VEGF表达有关,VEGF可能通过增加iNOS的表达促进肿瘤微血管形成。     

二十碳五烯酸对大鼠角膜新生血管血管内皮生长因子及其受体表达的抑制作用

目的 探讨二十碳五烯酸(eicosapentaenoic acid, EPA)对大鼠角膜新生血管(corneal neovascularization, CNV)血管内皮生长因子(VEGF)及其受体Flk-1表达的影响及作用机制.方法 78只SD大鼠按随机数字表法分为碱烧伤0.02 mg EPA治疗组(A组, 24只)、碱烧伤0.03 mg EPA治疗组(B组, 24只)、碱烧伤对照组(C组, 24只)、正常组(D组, 6只), 除正常组外,均选用右眼制作碱烧伤模型.A、B、C组碱烧伤后立即分别球结膜下注射0.02 mg/0.04 ml EPA、0.03 mg/0.04 ml EPA、0.04 ml生理盐水.每日裂隙灯显微镜下观察角膜水肿、新生血管情况.碱烧伤后1、4、7、14 d,用免疫组织化学方法检测角膜新生血管内皮细胞CD34表达,用逆转录聚合酶链反应(RT-PCR)及蛋白印迹法分别检测角膜VEGF的mRNA表达及Flk-1的蛋白表达.结果 碱烧伤7 d和14 d,角膜新生血管相对面积A组:(15.80±6 43)%、(11.06±2.14)%, B组:(16.10±7.41)%、(11.06±2.51)%,均显著少于C组:(84.74±7.77)%、(89.63±7 50)% (P<0.05).碱烧伤后7 d,C组CD34在CNV内皮细胞强阳性表达,A、B组未见CNV内皮细胞,CD34无表达.C组Flk-1蛋白及VEGF的mRNA表达,碱烧伤后1 d最高,持续高表达至4 d,随后逐渐下降.碱烧伤4 d,A、B组VEGF的mRNA表达及Flk-1的蛋白表达显著低于C组(P<0.05).结论 EPA能通过VEGF途径,抑制VEGF及其受体Flk-1的表达,从而显著抑制角膜新生血管的生长.     

穿山龙总皂苷对CIA大鼠滑膜血管新生的作用

目的:探讨穿山龙总皂苷对胶原诱导性关节炎(collagen-induced arthritis,CIA)大鼠滑膜血管新生及血管内皮生长因子(vascular endothelial growth factor,VEGF)表达的作用.方法:42只Wistar大鼠随机分为7组:正常对照组(A组)、CIA模型组(B组)、雷公藤组(C组)、穿山龙总皂苷高剂量组(D组)、穿山龙总皂苷中剂量组(E组)、穿山龙总皂苷低剂量组(F组)和薯蓣皂苷元组(G组),每组6只大鼠.B-G组大鼠均建立CIA大鼠模型,待模型成功建立后,C-G组大鼠分别给予相应的药物灌胃,连续21d.采用免疫组织化学染色法检测关节滑膜的微血管密度(MVD)和VEGF的表达.结果:CIA模型组大鼠滑膜MVD和VEGF的表达显著高于正常对照组(P＜0.01);C-G组大鼠滑膜MVD和VEGF的表达明显低于模型组(P＜0.01),且各治疗组间比较无显著差异(P＞0.05).结论:穿山龙总皂苷可能通过降低关节滑膜VEGF的表达发挥抑制滑膜血管新生的作用.     

长时间应用非那雄胺对老年大鼠前列腺组织的影响

目的评价长时间应用非那雄胺对老年大鼠前列腺组织中Bcl-2、Bax、CD34及一氧化氮合成酶（eNOS）表达的影响。方法雄性老年大鼠喂饲非那雄胺60d（20只,A组）和20d（20只,B组）,设喂饲生理盐水大鼠为对照组（20只,C组）,比较三组Bcl-2、Bax、CD34及eNOS的表达。结果与C组相比,A组及B组Bcl-2、CD34及eNOS表达下降,Bax表达上升（〈0.05）;B组和A组比较,CD34,eNOS表达下降（〈0.05）。结论非那雄胺可以通过上调Bax和下调Bcl-2的表达促进大鼠前列腺增生组织细胞凋亡,同时可以减少前列腺组织中微血管密度,长时间应用效果更佳。     

强力霉素对碱烧伤后角膜新生血管生长的影响

目的 探讨强力霉素对碱烧伤后角膜新生血管(CNV)形成及角膜血管内皮生长因子(VEGF)的影响.方法 将35只健康SD大鼠随机选取5只,为A组(正常组).余30只大鼠行右眼角膜碱烧伤,建立角膜新生血管动物模型,将其随机平分为B组(实验对照组)和C组(实验干预组).分别于3d,7d,14d裂隙灯下观察各组CNV的生长情况,计算新生血管面积,并采用免疫组化法检测大鼠角膜组织中VEGF的表达情况.结果 A组没有CNV生成,C组和B组相比CNV的生长明显受到了抑制;免疫组织化学染色结果示:A组VEGF微弱表达,B组和C组的表达明显高于A组,C组VEGF的表达低于B组,且差异具有统计学意义(P<0.05).结论 强力霉素可有效抑制角膜碱烧伤后CNV的生成及角膜组织中VEGF的表达.     

睾酮对血管内皮生长因子及其受体在大鼠前列腺组织中表达的影响

目的　探讨睾酮对血管内皮生长因子 (VEGF)及其受体之一 (FL K- 1)在前列腺组织中表达的影响。方法　分别在摘取大鼠睾丸后 7天及以后注射不同剂量的睾酮 ,HE染色观察前列腺的组织学变化 ,免疫组化SP法检测 VEGF和 FL K- 1在大鼠前列腺腹侧叶的蛋白表达。结果　正常大鼠前列腺可见多种生长状态上皮 ,VEGF和 FL K- 1蛋白在增生活跃上皮及间质的血管内皮上有阳性表达 ;去势可导致大鼠前列腺腹侧叶重量减轻(P<0 .0 5 ) ,组织学表现为上皮组织萎缩 ,VEGF和 FL K- 1在前列腺上皮中的蛋白表达明显降低 (P<0 .0 5 ) ;注射睾酮后 ,前列腺重量逐渐增加 (P<0 .0 5 ) ,组织学表现为上皮增生逐渐活跃 ,VEGF和 FL K- 1在前列腺上皮中的蛋白表达逐渐增强 (P<0 .0 5 )。结论　睾酮是维持大鼠前列腺腹侧叶生长和发育所必需的 ,睾酮可能通过正向调节VEGF及其受体 (FL K- 1)的蛋白表达来刺激前列腺组织的生长     

爱普列特对老年大鼠前列腺增生组织中微血管的影响

目的 探讨新型5α-还原酶抑制剂爱普列特对老龄雄性SD大鼠前列腺增生组织的微血管的影响及作用机制。方法将70只已增生老龄雄性SD大鼠随机分为爱普列特大剂量组（20只）、小剂量组（20只）、非那雄胺组（20只）及对照组（10只）,并分别采用免疫组化SP法和SABC法检测、对比各组大鼠前列腺增生组织中内皮型一氧化氮合酶（eNOS）和CD34的表达情况。结果爱普列特大剂量组、小剂量组及非那雄胺组MVD值（435±2．20、6．25±129、4．90±129）及eNOS（72．27±4850、163.89±91．40、144．82±8078）均明显低于对照组（8．00±298、293．58±1160）（均P〈0.05）;而且爱普列特大剂量组MVD值明显低于小剂量组（P〈0.05）,eNOS明显低于小剂量组及非那雄胺组（P〈0．05）。结论爱普列特对大鼠前列腺增生组织中血管的生成具有明显的抑制作用,其可能是通过下调eNOS及CD34的表达来实现的。     

Molecular mechanism of limbs’ postischemic revascularization improved by perindopril in diabetic rats

Background Currently, there are still divergent opinions about the mechanisms of the impaired neovascularization in diabetic subjects. Due to the remarkable therapeutic effect of angiotensin-converting enzyme inhibititors （ACEIs） on the reduction of blood pressure and the protection of target organs, the clinical application of this kind of drugs is very widespread. However, it is still not clear about the role and related molecular pathway of this kind of drugs in the limbs＇ postischemic revascularization. It is of major therapeutic importance to resolve these questions. This study aimed to investigate the reasons of the impaired angiogenesis in the hind limbs of rats with diabetic ischemia, the role and related molecular mechanisms of ACEI in postischemic revascularization.
Methods Hind limbs ischemia was induced in diabetic rats by right femoral artery excision. Diabetic rats were randomly allocated to one of the following treatments for 4 weeks： ACEI by perindopril; perindopril in combination with a nitric oxide synthase （NOS） inhibitor; perindopril in combination with bradykinin （BK）-B1 receptor （BIR） antagonist or saline. The differences of angiogenesis, the mRNA and protein expression of endothelial nitric oxide synthase （eNOS）, vascular endothelial growth factor （VEGF） and basic fibroblast （bFGF）, constitutive nitric oxide synthase （cNOS） activity and nitric oxide （NO） content were observed after treatment.
Results In non-ischemic hind limbs, no significant changes in capillary density, or the mRNA and protein expression of eNOS, VEGF and bFGF, or the NO content and the cNOS activity were observed among all groups. On the contrary, in ischemic hind limbs, the capillary density in diabetic rats decreased by 27% when compared with the control rats, so did the mRNA and protein expression of eNOS, VEGF and bFGF, or the NO content and the cNOS activity （P 〈0.05）. The capillary density was increased by 1.65-fold in the perindopril treatment group in reference to     

睾酮对血管内皮生长因子及其受体的大鼠前列腺组织中表达的影响

OBJECTIVE: To investigate the effects of testosterone on VEGF and FLK-1 protein expression in the ventral prostate of Rat. METHOD: SD rats were castrated, and 7 days later they were injected with different doses of testosterone. The histological changes were observed with the use of HE staining, and the protein expression of VEGF, FLK-1 were measured by immunohistochemical test. RESULTS: In the normal ventral prostate, different growth forms of epithelium were observed. In the castrated group, the proteins of VEGF, FLK-1 were positive in growth active epithelium and vascular endothelium; the weight of prostate decreased (P < 0.05); the histological appearance was epithelial atrophy, and there was significantly decreased protein expression of VEGF, FLK-1 in the prostatic epithelium (P < 0.05). It was found that testosterone injection stimulated prostatic hyperplasia gradually The histological changes were epithelial progressive proliferation. And a gradually increased protein expression of VEGF, FLK-1 in the prostatic epithelium was detected (P < 0.05). CONCLUSION: Testosterone can stimulate prostatic growth probably by upregulating the protein expression of VEGF and FLK-1.     

爱普列特减少经尿道前列腺汽化电切术中出血的作用研究

目的:探讨术前服用非竞争性5α-还原酶抑制剂爱普列特减少经尿道前列腺汽化电切术(transurethraluaporization of the prostate,TUVP)术中出血的作用。方法:将拟行TUVP的前列腺增生症(benign prostatic hyper-plasia,BPH)患者84例随机分为爱普列特治疗组和空白对照组,每组42例,计算术中出血量;免疫组织化学SP法检测前列腺组织内皮型一氧化氮合酶(eNOS)及VEGF蛋白的表达。结果:治疗组eNOS的蛋白表达较对照组减少31.5%,治疗组VEGF的表达阳性率明显低于对照组的表达阳性率(P<0.05)。爱普列特治疗组术中失血量(4.2±1.5)ml/g,空白对照组(7.1±2.3)ml/g,差异有显著性意义(P<0.05)。结论:术前服用爱普列特可抑制前列腺组织内VEGF蛋白和eNOS蛋白表达,抑制前列腺组织血管生成,减少TUVP术中出血。     

淫羊藿苷对动脉性ED模型大鼠阴茎海绵体压力和一氧化氮合酶亚型表达的影响

目的　建立动脉性勃起功能障碍大鼠模型 (arteriogenicerectiledysfunction ,A -ED) ,研究淫羊藿苷 (Icariin)对A -ED大鼠勃起功能和一氧化氮合酶 (NOS)三种亚型表达的影响。方法　 4 0只Wistar大鼠随机分为假手术组 (A组 )、A -ED组 (B组 )、A -ED低剂量淫羊藿苷治疗组 (C组 )和AED高剂量淫羊藿苷治疗组 (D组 )。结扎大鼠双侧髂内动脉建立A -ED动物模型后 ,C组和D组每天口饲不同剂量的淫羊藿苷 ( 5mg/kg ,10mg/k) ,A组和B组口饲等体积的生理盐水。 30d后 ,通过检测各组大鼠阴茎海绵体压力 (ICP)变化评估淫羊藿苷对大鼠勃起功能的效果 ,切取阴茎海绵体组织 ,通过逆转录 -PCR和Western印迹方法检测N0S亚型的表达变化。结果　建立A -ED模型 30d后 ,B组ICP较手术前显著降低 ,N0S三种亚型的表达水平也显著降低。经淫羊藿苷治疗后 ,C组和D组的ICP比B组明显升高 (P <0 .0 1) ,且D组较C组增高效果明显 ;C组和D组的eNOS表达水平较之B组有所增高 ,与ICP的变化有相同的趋势。C组的iNOS表达水平有一定程度的升高。治疗后nNOS表达水平没有明显增高。结论　经淫羊藿苷治疗后大鼠勃起功能显著改善 ,这种功能改善与eN0S的表达增加有相同的趋势 ,提示淫羊藿苷可能通过恢复eN0s的表达来改善A -ED模型的勃起功能。     

血管内皮细胞生长因子基因转染血管内皮祖细胞移植促进缺血皮瓣存活的实验研究

目的探讨VEGF165基因转染血管内皮祖细胞(EPCs)移植促进缺血皮瓣的血管新生,提高皮瓣存活率。方法体外分离、培养人脐血中EPCs,利用脂质体介导血管内皮细胞生长因子165(VEGF165)基因体外转染EPCs,然后移植于裸鼠随意皮瓣,皮瓣早期断蒂。结果脐血中分离培养的EPCs表达CD34、KDR及CD133,VEGF165基因转染EPCs体外及体内检测均有VEGF165蛋白的表达。转染VEGF165基因的EPCs组和EPCs组移植裸鼠皮瓣后,EPCs整合到缺血部位新生血管中,与对照组的皮瓣存活率分别为97 2% ±2 8%、60 3% ±2 1%、34 2% ±1 8% (P<0 05 ),而且前二组毛细血管密度、血流灌注差异均有统计学意义(P<0 05),较对照组均有明显改善(P<0 05)。术后第7d时三组皮瓣中的EPCs密度分别为136个/mm2 ±10个/mm2、75个/mm2 ±6个/mm2、0个/mm2 (P<0 05 ); 第11天时EPCs密度分别为305个/mm2 ±26个/mm2、199个/mm2 ±18个/mm2、0个/mm2 (P<0 05)。结论脐血中的EPCs体外培养后移植体内可促进缺血皮瓣的血管新生,提高存活率,而转染VEGF165基因的EPCs具有更强大的促血管新生的作用。     

Transplantation of VEGF165-gene-transfected endothelial progenitor cells in the treatment of chronic venous thrombosis in rats

Background The organization and recanalization of thrombi is a dynamic and complex process. The aim of this research was to study the cotherapeutic effect of stem cell transplantation and gene transfection on chronic venous thrombosis. Methods We constructed a recombinant adenoviral vector carrying the vascular endothelial growth factor 165 （VEGF165） gene by using the pAdEasy system, which was subsequently identified and amplified. Simultaneously, endothelial progenitor cells （EPCs） were isolated from rat bone marrow using Ficoll, cultured in EBM-2MV medium, and identified. Then, the cells were transfected with the recombinant Ad-VEGF165. The EPCs were labeled with 1 ,1＇-dioctadecyl-3,3,3＇,3＇-tetramethylindocarbocyanine （Dil） before transplantation. A rat model of chronic vein thrombosis was developed by partial ligation of the inferior vena cava. The rats were randomly divided into 4 groups （n=25, each）： A, Ad-VEGF165/EPC-transplantation group received 1 ml （10^6） of Ad-VEGF165/EPCs; B, EPC-transplantation group received 1 ml （10^6） of EPCs; C, Ad/EPC-transplantation group received 1 ml （10^6） of Ad/EPCs; D, control group received 1 ml of the transplantation medium. The thrombi and adjacent caval walls were harvested 28 days after transplantation; real-time quantitative polymerase chain reaction was used to detect the expression level of vascular endothelial growth factor （VEGF） mRNA; and western blotting was used to measure changes in VEGF protein expression. Hematoxylin-eosin staining and immunohistochemical staining were performed to detect recanalization. Neovascularization was detected by immunohistochemical staining using the antibody for von Willebrand factor （vWF）, which is a component of endothelial cells.The capillary density was quantitatively determined by counting the capillaries under a high-power microscope. Results The Ad-VEGF165 was constructed, and bone-marrow-derived EPCs were cultivated and successfully identified. We determined the optimum transfection ratio that promoted the growth of EPCs. After transfection, the EPCs secreted the VEGF protein. After transplantation, the in vivo survival of EPCs and their differentiation into endothelial cells were determined by detecting the fluorescence associated with the Dil stain. VEGF mRNA was expressed in groups A, B, C and D after transplantation, and the VEGF mRNA level in group A was significantly higher than those in groups B, C and D （P〈0.05）; the VEGF mRNA levels in groups B and C were significantly higher than those in group D （P〈0.05）, and there was no statistical significance between the VEGF mRNA levels in groups B and C. The recanalization capillary density in group A was significantly higher than those in groups B, C （P 〈0.05） and D （P 〈0.01）; the recanalization capillary densities in groups B and C were significantly higher than that in group D （P 〈0.05）. Moreover, there was no statistical significant difference between the values for groups B and C. Conclusions The EPCs were successfully transfected by Ad-VEGF165. A suitable transfection ratio can improve the efficiency of EPCs and the possibility of promotion of angiogenesis after transplantation. Transfected EPCs caused accelerated organization and recanalization of vein thrombi.