Role of pigment epithelium-derived factor on proliferation and migration of choroidal capillary endothelium induced by vascular endothelial growth factor in vitro

Background Pigment epithelium-derived factor （PEDF） is expressed in several normal organs and identified as an inhibitor of neovascularization. In the present study, we investigated the effect of PEDF in an in vitro model of ocular choroidal neovascularization. Methods Microdissection was used to isolate the human choroidal endothelial cells （CECs）, followed by the use of superparamagnetic beads （Dynabeads） coated with the CD31 antibody, which selectively binds to the endothelial cell surface. The mitogenic and motogenic effects of vascular endothelial growth factor （VEGF） on cultured choroidal capillary endothelial cells were examined in the presence or absence of PEDF （1, 10, 100, and 1000 ng/ml） using cell counts and migration assays. Results Cells bound to the beads were isolated using a magnetic particle concentrator and they were successfully cultured and characterized to be endothelial cells that possessed greater than 95% immunoreactivity to von Willebrand factor. PEDF suppressed the proliferation and migration of VEGF-induced choroidal capillary endothelial cells. However, the concentration of PEDF which we used has little effect on normal CECs. Conclusions PEDF played an important role on the growth and migration of VEGF-stimulated choroidal endothelial cell These findings suggest that PEDF may be an effective approach to the treatment of choroidal neovascular disorders.     

超声微泡介导肾小管上皮细胞β-半乳糖苷酶基因的转导

目的：以β-半乳糖苷酶基因作为报告基因,探讨超声微泡介导在人肾近端小管上皮细胞（HKCs）中的转染效率和安全性。方法：体外培养HKCs,分为单纯超声组、单纯微泡组、裸质粒组、超声+质粒组、微泡+质粒组、超声+微泡+质粒组以及VigoFect+质粒组。超声+微泡+质粒组应用微泡和Plenti6-LacZ质粒转导HKCs后,给予不同强度不同时间超声辐照。采用X-gal染色观察细胞基因转导效率,台盼蓝染色观察细胞存活率,Hochest染色观察细胞凋亡率。结果：超声+微泡+质粒组转染效率高于其他各组;与VigoFect+质粒组相比无统计学差异（P>0.05）。随超声声强增加和辐照时间延长,HKCs存活率下降,凋亡率升高。声强为0.3 W/cm2时,辐照时间为60 s时,细胞存活率和转导效率均较高,而细胞凋亡率较低。结论：在适当超声强度和辐照时间条件下,超声微泡可安全、有效地促进肾小管上皮细胞的基因转染,是一种较理想的基因转导方法,这为肾脏病的基因治疗提供了实验基础。     

血清PEDF及PEDF基因启动子区多态性与2型糖尿病患者微量白蛋白尿的相关性

目的:探讨福建地区汉族2型糖尿病患者血清色素上皮衍生因子水平(pigment epithelium-derived factor,PEDF)及PEDF基因启动子区rs1294385单核苷酸多态性与微量白蛋白尿的关系?方法:471例2型糖尿病患者根据尿白蛋白/肌酐比值(urinary albumin to creatinine ratio,UACR)分为正常组(UACR<30 μg/mg,NAU组)246例?微量白蛋白尿组(30 μg/mg≤UACR<300 μg/mg,MAU组)225例,使用PCR-RFLP方法检测PEDF基因启动子区rs1294385的多态性,同时检测血清PEDF水平及空腹血糖?空腹胰岛素?糖化血红蛋白?血脂等指标?结果:MAU组的血清PEDF水平高于NAU组,差异有统计学意义(P < 0.05);偏相关分析显示血清PEDF水平与UACR呈正相关(P < 0.05);PEDF基因启动子区rs1294385的基因型(GG型?GA型和AA型)和等位基因(G/A)在NAU?MAU两组间的分布存在差异,且差异有统计学意义(P < 0.05);GA基因型出现微量白蛋白尿的风险是GG基因型的1.838倍,GA+AA基因型出现微量白蛋白尿的风险是GG基因型的1.862倍,差异有统计学意义(P < 0.05)?结论:2型糖尿病患者血清PEDF水平随微量白蛋白尿的出现而增高;福建地区汉族2型糖尿病患者PEDF基因启动子区rs1294385多态性与微量白蛋白尿明显相关,携带A等位基因可能增加2型糖尿病患者发生微量白蛋白尿的机率?     

色素上皮细胞源性因子影响黑色素瘤的实验研究

目的研究色素上皮细胞源性因子(PEDF)在体内、外的高表达对黑色素瘤细胞生长、转移等生物学行为的影响。方法用脂质体转染pcDNA3-PEDF质粒导入黑色素瘤A375细胞,G418筛选,蛋白质印迹鉴定。四甲基偶氮唑蓝(MTT)分析体外PEDF转染肿瘤细胞的增殖。以PEDF高表达的肿瘤细胞皮下注射于裸鼠,检测原发性肿瘤的生长。采用抗鼠CD31单克隆抗体免疫组化检测肿瘤微血管密度。苏木精-伊红染色检测肺转移。结果体外研究显示,PEDF显著抑制黑色素瘤A375细胞的增殖;在裸鼠皮下接种高表达PEDF的肿瘤细胞后,与对照细胞比较,高表达PEDF的细胞在裸鼠皮下致瘤能力减弱,肿瘤生长明显减慢;CD31染色显示高表达PEDF的肿瘤微血管密度明显降低[(34±3.75):(12.37±3.52)(P<0.01)],且苏木精伊红染色发现肿瘤肺转移也被显著抑制。结论PEDF可以显著抑制黑色素瘤的新生血管生成,抑制肿瘤的生长和转移,可能为治疗黑色素瘤提供实验室依据。     

腺相关病毒介导色素上皮衍生因子转染人虹膜色素上皮细胞的体外研究

目的探讨以腺相关病毒(AAV)为载体,对体外培养的人虹膜色素上皮(IPE)细胞进行色素上皮衍生因子(PEDF)转染,获得高效表达PEDF转基因细胞的可行性。方法构建携带PEDF基因的重组AAV载体AAV-PEDF,体外培养人IPE,用1×106pfu的AAV-PEDF按感染复数(MO I)为0、2、10和20分别感染体外培养的IPE细胞;荧光显微镜下观察细胞绿色荧光蛋白表达情况;流式细胞术检测细胞转染效率;RT-PCR和W estern b lotting法鉴定PEDF在IPE细胞中的表达。结果 AAV-PEDF转染后,IPE细胞生长正常,用荧光显微镜、RT-PCR和W estern b lotting均检测到PEDF表达。在MO I为20时,细胞感染阳性率达64.22%。结论 AAV-PEDF能有效地转染体外培养的IPE细胞并有效表达PEDF。     

脉络膜新生血管患者房水中血管内皮生长因子和色素上皮衍生因子的浓度

目的:研究血管内皮生长因子(VEGF)和色素上皮衍生因子(PEDF)在活动性脉络膜新生血管膜(CNV)患者房水中的表达。方法:应用酶联免疫吸附测定法对32例活动性CNV患者和10例白内障患者(对照组)的房水标本进行VEGF和PEDF检测。结果:CNV患者房水中的VEGF为(523.0±273.7)pg/m l,PEDF为(16.58.±13.11)ng/m l;对照组患者房水中的VEGF为(108.3±72.3)pg/m l,PEDF为(0.35±0.57)ng/m l。两组间的VEGF和PEDF均有显著性差异(均P=0.000)。结论:活动性CNV患者房水中VEGF和PEDF增高,可能与脉络膜新生血管的形成有关。     

病理性近视脉络膜新生血管的治疗

病理性近视早期即可出现眼底病变且进行性加重,可导致视功能明显受损,其中脉络膜新生血管的发生是视力丧失的主要原因。文章对病理性近视的患病率、危害、自然转归、影响因素和治疗方法进行综述,着重探讨抗血管内皮生长因子药物治疗的进展。     

血浆色素上皮衍生因子及血管内皮生长因子含量与2型糖尿病视网膜病变相关性的研究

目的 探讨2型糖尿病患者血浆色素上皮衍生因子(pigment epithelium-derived factor,PEDF)和血管内皮生长因子(vascular endothelial growth factor,VEGF)浓度变化与糖尿病视网膜病变(diabetic retinopathy,DR)的关系.方法 选择门诊及住院2型糖尿病患者71例分为3组:2型糖尿病无视网膜病变(diabetes mellitus without retinopathy)即DM无DR组22例、2型糖尿病并非增殖期视网膜病变(diabetes mellitus non-proliferative DR)即DM伴NPDR组33例、2型糖尿病并增殖期视网膜病变(diabetes mellitus with proliferative DR)即DM伴PDR组16例.另选取正常志愿者(非糖尿病组)13例作为对照.收集年龄、病程等数据,采用酶联免疫吸附测定(enzyme-linked immunosorbent assay,ELISA)法检测血浆中PEDF和VEGF水平.结果 与非糖尿病组比较,DM伴NPDR和DM伴PDR组血浆中PEDF水平均明显升高(P＜0.05).2型糖尿病患者中,随着DR的发生发展,血浆中PEDF含量明显上升(P＜0.05).2型糖尿病患者各组血浆中VEGF含量差异均无统计学意义(P＞0.05),与DR的发生发展亦无明显相关性.DR的发生与2型糖尿病病程有明显的相关性,而与性别、年龄无明显相关性.结论 血浆中PEDF含量随着DR发生发展呈现增加的趋势,这可能与2型糖尿病病程的延长以及机体胰岛素抵抗程度增加有关.     

Ultrasound-triggered microbubble destruction in combination with cationic lipid microbubbles enhances gene delivery

This study aimed to examine the preparation of cationic lipid microbubble(CLM),and evaluate its physical and chemical properties and toxicity,measure the gene transfection efficiency by ultrasound triggered microbobble destruction(UTMD) in combination with CLM.The CLM was prepared by the method of the thin film hydration,and its morphology was observed under the electron microscopy at 1st,3rd,7th,10th,and 14th day after preparation,respectively.The size,Zeta potential and stability of CLM were tested.The acute toxicity of CLM was assessed.The green fluorescent protein gene(EGFP) transfection efficiency was evaluated.The experiment grouping was as follows:naked plasmid group(P group),ultrasonic irradiation plus naked plasmid group(P-US group),naked plasmid plus CLM group(P-CLM group),naked plasmid plus ultrasound and CLM group(UTMD group).The expression of EGFP was detected by fluorescent microscopy and flow cytometry.The results showed that CLMs were spherical in shape,with the similar size and good distribution degree under the light and electron microscopies.The size of CLMs was varied from 250.4±88.3 to 399.0±99.8 nm and the Zeta potential of CLMs from 18.80±4.97 to 20.1±3.1 mV.The EGFP expression was the strongest in the UTMD group,followed by the P-CLM group,P-US group and P group.Flow cytometry results were consistent with those of fluorescent microscopy.The transfection efficiency was substantially increased in the P-US group,P-CLM group and UTMD group as compared with that in the P group,almost 7 times,10 times and 30 times higher than that in the P group respectively.It is suggested that CLMs prepared by the method of thin film hydration are uniform in diameter,and proved non-toxic.UTMD combined with CLM can significantly increase the transfection efficiency of EGFP to targeted cells.     

病理性近视伴脉络膜新生血管的特点及其抗VEGF药物治疗

脉络膜新生血管是病理性近视患者常见的视力下降的重要原因之一,常引起不可逆的中心视力丧失。该文主要对病理性近视的流行病学、继发于病理性近视的脉络膜新生血管的病理机制、临床表现及其抗VEGF药物的治疗进行综述。     

病理性近视伴脉络膜新生血管的特点及其抗VEGF药物治疗

脉络膜新生血管是病理性近视患者常见的视力下降的重要原因之一,常引起不可逆的中心视力丧失.该文主要对病理性近视的流行病学、继发于病理性近视的脉络膜新生血管的病理机制、临床表现及其抗VEGF药物的治疗进行综述.     

Efficient Gene Delivery to Myocardium with Ultrasound Targeted Microbubble Destruction and Polyethylenimine

The aim of present study was to evaluate the feasibility and efficiency of enhanced green fluorescent protein （EGFP） gene delivery to myocardium in vivo by ultrasound targeted microbubble destruction （UTMD） and polyethylenimine （PEI）. SonoVue/DNA and PEI/DNA/SonoVue complexes were prepared. Gel electrophoresis analysis was performed to determine the structural integrity of plasmid DNA or PEI/DNA after UTMD. Solutions of plasmid DNA, SonoVue/DNA, PEI/DNA complexes or PEI/DNA/SonoVue complexes were respectively transduced into BALB/c mice hearts by means of transthoracic ultrasound irradiation. Mice undergoing PBS injection, plasmid injection or PEI/DNA complexes injection without ultrasound irradiation served as controls. Gene expression in myocardium was detected 4 days after treatment. Cryosections and histological examinations were conducted. Electrophoresis gel assay showed no damage to DNA or PEI/DNA complexes after UTMD. When the heart was not exposed to ultrasound, the expression of EGFP was observed in the subendocardial myocardium obviously. The strongest expression was detected in the anterior wall of the left ventricle when the heart was exposed to ultrasound alone. Injection of PEI/DNA complexes and UTMD resulted in the highest transfection efficiency and the distributional difference of EGFP was not obvious. No tissue damage was seen histologically. In conclusion, a combination of UTMD and PEI was highly effective in transfecting mice hearts without causing any apparently adverse effect. It provides an alternative to current clinical gene therapy and opens a new concept of non-viral gene delivery for the treatment of cardiac disease.     

Targeting therapy of choroidal neovascularization by use of polypeptide- and PEDF-loaded immunoliposomes under ultrasound exposure

Pigment epithelium derived factor (PEDF) has been proven to be an effective drug for the treatment of choroidal neovascularization (CNV).However,the lack of ideal administration route is the biggest bottleneck preventing PEDF from wider clinical use.In this study,we developed a novel PEDF-carrying system which employed immuno-nano-liposomes (INLs) under ultrasound exposure.PEDF-loaded INLs were prepared by conjugating nanoliposomes to the peptide ATWLPPR specifically targeting the receptor-2 for vascular endothelial growth factor (VEGFR-2) and reversely encapsuling PEDF.RF/6A cells were incubated with PEDF-loaded INLs.CNV models of BN rats were injected with PEDF-loaded INLs.MTT assay was used to evaluate the cytotoxicity of the INLs on RF/6A cells.Flow cytometry was conducted to detect the apoptotic rate of cells.Laser scanning confocal microscopy was employed to observe the binding and transmitting process of PEDF-loaded INLs and to calculate the area of CNV in the rat model.The results showed that the PEDF-loaded INLs could exclusively bind to CNV but not to the normal choroidal vessels.The CNV area was significantly decreased in PEDF treatment groups in comparison with control group (P<0.05).Moreover,PEDF-loaded INLs exposed under ultrasound were more efficient in reducing the CNV area (P<0.05).It was concluded that INLs in combination with ultrasonic exposure can transmit PEDF into cytoplasma with high specificity and efficiency,which strengthens the inhibitory effects of PEDF on CNV and reduces its side effects.PEDF-loaded INLs possibly represent a new treatment paradigm for patients with ocular neovascularization.     

糖尿病足患者血清色素上皮衍生因子水平的变化及意义

目的:探讨糖尿病足患者血清色素上皮衍生因子(PEDF)水平变化及其在糖尿病足中发生发展的意义。方法:纳入72例糖尿病足患者,同时选择66例无并发症的2型糖尿病患者及50例健康人作对照。分别测量身高、体重、腰围(WC)、血压,计算体重指数(BMI);测定空腹血清PEDF、血糖(FPG)、血脂和糖化血红蛋白(HbAlc)。结果:(1)糖尿病足组血清PEDF水平明显高于2型糖尿病对照组(6.27±2.03vs.5.13±1.32μg/mL,P<0.05),2型糖尿病对照组明显高于正常对照组(3.36±1.27μg/mL)。(2)Pearson相关分析显示,糖尿病足组血清PEDF水平与BMI、WC、收缩压(SBP)、空腹血糖(FPG)、甘油三脂(TG)、HbAlc呈正相关,与高密度脂蛋白胆固醇(HDL-c)呈负相关。(3)逐步多元线性回归分析显示,BMI、TG和HbAlc是糖尿病足血清PEDF水平的独立影响因素。结论:糖尿病足患者血清PEDF水平明显升高,提示PEDF可能参与了糖尿病足的发生和发展。     

内皮抑素对小鼠脉络膜新生血管抑制作用的信号通路分析

目的探讨内皮抑素对C57BL/6J小鼠脉络膜新生血管抑制作用的基因表达及作用机制。方法应用532 nm固体激光机,制造C57BL/6J小鼠脉络膜新生血管模型,分为空白组、对照组和实验组。其中空白组不做任何处理,对照组玻璃体腔内注射生理盐水2μL;实验组玻璃体腔内注射内皮抑素2μL(0.01 mg)。将对照组和实验组小鼠组织选取4个样本进行杂交及基因芯片检测。比较实验组和对照组基因表达的差异,选取其中表达差异大于1.5倍且P≤0.05的基因。结果免疫组织化学染色可见实验组新生血管表达明显低于对照组。实验组与对照组相比上调的基因有116个,下调的基因有106个。通过KEGG(Kyoto Encyclopedia of Genes and Genomes)数据库对上述差异基因经行分析后发现,实验组与对照组相比下调处于前10位的通道有:细胞骨架激动蛋白的校准、白细胞穿越内皮细胞层、金黄色葡萄球菌感染、Fc epsilon RI信号通路、Fc gamma R信号调理吞噬作用、Toll样受体信号通路、2型糖尿病、子宫内膜癌、吞噬体、非小细胞肺癌;处于上调前几位的通道有:细胞外基质受体相互作用、叶酸的一碳单位、肥厚性心肌病、扩张型心肌病、组氨酸新陈代谢、黏着斑、心肌细胞收缩。结论由通道功能分析可以推测,内皮抑素可能通过抑制内皮细胞的活性及移行并协同抑制免疫系统,进而抑制新生血管的生成。     

2型糖尿病患者PEDF基因启动子区多态性与非酒精性脂肪肝病的相关性

目的探讨福建地区汉族2 型糖尿病患者血清色素上皮衍生因子水平及色素上皮衍生因子基因启动子区-358 位点单
核苷酸多态性与非酒精性脂肪肝病的关系。方法选择2 型糖尿病患者共452 例,按有无合并非酒精性脂肪肝病分为性别、
年龄比例相近的DM1 组（合并非酒精性脂肪肝病）282 例,DM2 组（不合并非酒精性脂肪肝病）170 例,采用聚合酶链反应
——限制性片段长度多态性（PCR-RFLP）技术检测色素上皮衍生因子基因启动子区-358 位点多态性,同时检测血清色素上
皮衍生因子水平及空腹血糖、空腹胰岛素、糖化血红蛋白等指标。结果DM1 组的血清色素上皮衍生因子水平高于DM2
组,差异有统计学意义（P<0.05）;以非酒精性脂肪肝病为因变量的二分类非条件Logistic 回归分析中,结果显示血清色素上
皮衍生因子作为独立影响因素影响2 型糖尿病患者非酒精性脂肪肝病的发生;色素上皮衍生因子基因启动子区
SNP-358G→A的基因型（GG型、GA型和AA型）和等位基因（G/A)在DM1、DM2 两组间的分布存在差异,有统计学意义（P<
0.05）;2 型糖尿病患者-358 位点GA基因型出现非酒精性脂肪肝病的风险是GG基因型的2.032 倍,GA+AA基因型出现非酒
精性脂肪肝病的风险是GG基因型的2.068 倍,差异有统计学意义（P<0.05）。结论血清色素上皮衍生因子水平是2 型糖尿
病患者发生非酒精性脂肪肝病的独立影响因素,血清色素上皮衍生因子水平的升高为胰岛素抵抗的反馈表现,可改善胰岛
素抵抗,保护胰岛素敏感性。2 型糖尿病患者的色素上皮衍生因子基因启动子区-358G→A多态性与非酒精性脂肪肝病有
关,携带A等位基因可能增加非酒精性脂肪肝病的易感性。
     

PEDF对人肺腺癌A549细胞增殖与凋亡的影响

目的探讨不同浓度色素上皮衍生因子( PEDF)作用不同时间对体外培养的人肺腺癌A549细胞增殖和凋亡的影响。方法用不同浓度(0、80、160、320、640 nmol/L)的重组人PEDF蛋白对体外培养的人肺腺癌细胞株A549进行干预,在处理24、48、72 h后,分别用MTT法检测PEDF对A549细胞增殖的抑制率并比较;在作用48 h后,以流式细胞仪检测技术计算、分析 A549细胞凋亡率。结果不同浓度PEDF(0、80、160、320、640 nmol/ L)干预A549细胞相同作用时间(24、48、72 h)情况下,随着PEDF 浓度的增加,PEDF 对 A549细胞的增殖抑制率递增(P <0.05);相同PEDF 浓度(80、160、320、640 nmol/ L)情况下,除了80、160 nmol/ L PEDF 作用24 h 和48 h 的细胞增殖抑制率间差异无统计学意义外,随着PEDF 作用时间的延长,PEDF 对A549细胞的增殖抑制率也基本呈递增趋势(P <0.05)。上述不同浓度的PEDF 处理A549细胞48 h,细胞凋亡率随着PEDF 浓度的升高呈递增趋势(P <0.05)。结论摇PEDF 在体外能抑制人肺腺癌细胞株A549的增殖并诱导其凋亡。PEDF 抑制细胞增殖作用可能和PEDF 浓度及作用时间有关,PEDF 诱导细胞凋亡作用的强弱也与PEDF 浓度有一定关系。     

重组人色素上皮衍生因子显著抑制血管内皮细胞增殖

目的通过原核表达,获得具有生物活性的人重组色素上皮衍生因子(PEDF).方法将PEDF基因构建到GST原核表达系统中,经过表达纯化,获得重组蛋白,采用Westem b1ot和质谱分析确证该重组蛋白,采用MTT法检测所获得的重组蛋白对人脐静脉内皮细胞增殖的抑制活性.结果获得了相对分子质量为46 000的重组人PEDF重组蛋白,该蛋白可显著抑制血管内皮细胞增殖.结论成功地经过原核表达获得了具有血管生成抑制活性的重组人色素上皮衍生因子.     

超声联合微泡造影剂携p53基因转染宫颈癌HeLa细胞的实验研究

目的 探讨超声联合微泡造影剂介导野生型p53(wtp53)基因转染宫颈癌HeLa细胞的可行性、效率性及作用效果.方法 以前期实验所筛选的超声辐照参数(300 kHz,0.5 W/cm~2,30 s)为实验条件,将HeLa细胞分为质粒组(A组)、质粒+超卢组(B组)、质粒+超声+微泡组(C组)、质粒+脂质体组(D组)、空白对照组(E组),分别进行处理.转染24～48 h后,收集各组细胞,荧光显微镜观察细胞基因转染效率、RT-PCR检测p53 mRNA表达,流式细胞仪检测细胞周期,M1Tr检测细胞增殖抑制情况.结果 荧光显微镜下见C、D组均有较多绿色荧光蛋白表达的细胞(转染率分别为14.15%和10.86%),B组仅有极少的荧光细胞(0.81%);A组和E组无荧光表达;RT-PCR结果 显示,C组和D组均可见特异性p53电泳条带,C组的电泳条带的光密度比值高于D组(P<0.05);流式细胞仪测细胞周期展示,转染野生型p53基因能使细胞周期出现明显的G_1期阻滞,C、D组与E组相比差异有显著性(P<0.05);MTT测定结果 显示c组细胞生长明显受抑,且随时间的延长,抑制程度逐渐增强.结论 适当浓度的微泡和优化的超声辐照条件可增强基因转染效率,野生型p53基阒能使HeLa细胞产生G_1期阻滞,抑制宫颈癌细胞生长.     

色素上皮衍生因子对鼠视网膜新生血管形成的保护作用

目的本课题通过小鼠视网膜新生血管动物模型观察玻璃体内注入色素上皮衍生因子(PEDF)对视网膜新生血管形成的影响,并探讨其治疗作用。方法选取鼠龄为7天的健康昆明小鼠28只(56只眼),随机分为4组:正常组、高氧组、PEDF干预组和对照生理盐水组,每组7只。正常对照组鼠在正常空气环境中饲养,其余3组鼠置于氧箱中,建立高氧诱导的视网膜新生血管动物模型。正常组鼠不做任何处理,PEDF干预组幼鼠在出生后第12天向玻璃体腔内注射PEDF 1μl,而对照生理盐水组注射相同体积的生理盐水。各组小鼠均在出生后第17天处死,摘除眼球制作标本,进行组织病理学观察。在光学显微镜下观察并计数突破视网膜内界膜的血管内皮细胞细胞核数目。采用CD31分子免疫组化方法鉴别视网膜内界膜与血管内皮细胞。结果正常对照组标本HE染色未见突破内界膜的内皮细胞核,高氧组和对照生理盐水组标本可见较多的突破内界膜的内皮细胞核,与正常组比较差异具有显著性(P<0.05),PEDF干预组的数目明显少于高氧组和对照生理盐水组,差异均具有显著性(P<0.05),且未见明显药物毒性反应。CD31分子免疫组化染色证实突破内界膜的细胞为血管内皮细胞。结论玻璃体内注入一定剂量的PEDF,能够有效抑制高氧诱导下的小鼠视网膜新生血管形成,PEDF有望成为防治血管增生性视网膜病变的一种有效的方法。