增生型糖尿病视网膜病变眼内液中血管内皮生长因子定量测定

目的：检测增生型糖尿病视网膜病变（PDR）患者房水和玻璃体中血管内皮生长因子（VEGF）水平。方法：应用酶联免疫吸附测定法（ELISA）。结果：房水VEGF含量,PDR患者（4例）较正常人升高,差异有显著性（P＜0.05）。玻璃体VEGF的含量,PDR患者（11例）较正常人（10例）升高,差异有显著性（P＜0.05）。结论：PDR患者房水和玻璃体中VEGF的含量升高,在PDR的病理过程中起一定的作用。     

糖尿病视网膜病变血浆与眼内液血管内皮生长因子的相关研究

目的 通过检测糖尿病性视网膜病变(DR)患者血浆、眼内液(房水、玻璃体)血管内皮生长因子(VEGF)含量，探讨其在DR发展变化中 的作用。 方法 采用双抗体夹心酶联免疫吸附试验ELISA法定量检测患者组及对照组血浆、房水、玻璃体VEGF含量。 结果 无糖尿病性视网膜病变(NDR)组血浆VEGF含量(34.47±1.76) pg/ml ，单纯型糖尿病性视网膜病变(BDR)组血浆VEGF含量(53.93±3.08) pg/ml，增生型糖尿病性视网膜病变(PDR)组血浆VEGF含量(53.36±3.28) pg/ml，对照组血浆VEGF含量(178.30±10.13) pg/ml，与实验组比较差异均有显著性的意义(P＜0.05)；PDR组房水VEGF含量(184.86±1260) pg/ml，对照组房水VEGF含量(90.06±18.32) pg/ml，两者比较差异有显著性的意义(P＜0.05)；PDR组玻璃体VEGF含量(741.70±92.02) pg/ml，对照组玻璃体VEGF含量(94.38±21.21) pg/ml，两者比较差异有显著性的意义(P＜0.05)。PDR组血浆VEGF与房水、玻璃体VEGF无相关关系(P＞0.05)，玻璃体VEGF与糖化血红蛋白(HbA1c)有正相关关系(r=0.9067,P＜0.01)。 结论 糖尿病患者血浆VEGF含量较正常人低，但与房水、玻璃体VEGF含量无关；增生型糖尿病性视网膜病变患者房水与玻璃体VEGF含量增高，玻璃体内VEGF含量增高与患者HbA1c值有关。 (中华眼底病杂志，2004，20：343-345)     

VEGF在PDR中的表达及作用的研究

目的:研究增殖性糖尿病视网膜病变(proliferative diabetic retinopathy,PDR)患者血液、房水、玻璃体中血管内皮生长因子(vascular endothelial growth factor,VEGF)含量的变化,探讨VEGF与PDR的关系,为抗VEGF药物治疗的给药途径及剂量等提供理论依据。方法:采用双抗体夹心酶联免疫吸附测定法定量检测无糖尿病视网膜病变(NDR)组,单纯性糖尿病视网膜病变(BDR)组,增殖性糖尿病视网膜病变(PDR)组患者和正常对照组血浆中VEGF含量,还检测PDR患者房水、玻璃体中和正常对照组房水、玻璃体中VEGF含量,并进行综合分析。试剂盒购自美国R&D公司,其质量和灵敏度相对较高。结果:PDR组房水中VEGF含量有增高趋势,但与正常对照组比较,无统计学差异(P>0.05)。PDR患者玻璃体中VEGF含量明显增高,与正常对照组比较差异非常显著(P<0.01)。PDR组自身血浆、房水、玻璃体中VEGF含量比较有逐渐增高趋势,三者之间有显著性差异(P<0.01)。正常对照组血浆、房水、玻璃体中VEGF含量三者之间无显著性差异(P>0.05)。血浆VEGF含量在正常对照组中最高,而玻璃体中VEGF含量在PDR患者中最高。结论:PDR患者眼内尤其是玻璃体中VEGF含量大幅度增高,可能对促进DR发展恶化起了关键性的作用。在正常人,VEGF更多地存在于血浆中发挥其生物学效应。在严重DR患者中,玻璃体中异常地出现大量VEGF,推测来自缺血缺氧的视网膜,并可能有向眼前段扩散的趋势。     

增生性糖尿病视网膜病变患者玻璃体内血管内皮生长因子的表达

目的 探讨增生性糖尿病视网膜病变(PDR)患者玻璃体内血管内皮生长因子(VEGF)的表达及相关影响因素.方法 病例对照研究.对50例(50只眼)接受玻璃体切除治疗的PDR患者进行分析.术中获取玻璃体标本,并用双抗体夹心酶联免疫吸附试验ELISA法对术中获取的玻璃体标本进行VEGF含量的定量检测,并分析增生性糖尿病视网膜病变患者玻璃体内VEGF的表达情况.平均随访9个月(6～26个月).用成组t检验比较PDR组和正常对照组玻璃体VEGF含量差异,以及硅油填充组与非硅油填充组VEGF含量差异.用方差分析方法比较PDR进展组、稳定组和好转组玻璃体VEGF含量有无差异.用单因素方差分析方法分析玻璃体VEGF含量对PDR术后疗效的影响.结果 PDR组玻璃体VEGF含量平均(592.4801±587.4267)ng/L,正常对照组玻璃体VEGF含量平均(131.3022±26.9192)ng/L.PDR组玻璃体VEGF含量高于对照组(t=3.2315,P＜0.05).术后PDR进展有10只眼(20%),稳定10只眼(20%),好转30只眼(60%).PDR进展组玻璃体VEGF含量显著高于PDR稳定和好转组(q=-3.3187,-4.0843;P＜0.05).术前未接受视网膜光凝组玻璃体VEGF含量显著高于接受全视网膜光凝或局部视网膜光凝组(q=-4.2187,-3.9672;P＜0.05).结论玻璃体VEGF表达与PDR严重程度有一定关系.术后PDR稳定或好转者玻璃体VEGF水平呈相对低表达.(中华眼科杂志,2009,45:206-209)     

新生血管性青光眼血管内皮生长因子和血小板衍生生长因子含量及其相关影响因素

目的 观察新生血管性青光眼（NVG）患者眼内血管内皮生长因子（VEGF）和血小板衍生生长因子（PDGF）含量,并分析其相关影响因素.方法 实验研究.NVG患者54 例（54眼）,其中视网膜中央静脉阻塞（CRVO）17眼,糖尿病性视网膜病变（DR）22眼,视网膜血管炎（Eales病）4眼,视网膜脱离（RD）术后4眼,未知原因7眼.虹膜新生血管Ⅰ级17眼,Ⅱ级12眼,Ⅲ级13眼,Ⅳ级12眼.36眼曾行视网膜光凝和（或）冷凝治疗.10只新鲜健康角膜供体眼作为正常对照组.抽取两组的房水和玻璃体液样本,采用酶联免疫吸附试验（ELISA）检测其中VEGF和PDGF含量.对NVG组和正常对照组VEGF和PDGF含量的比较采用Mann-Whitney U检验,不同原发病、不同等级虹膜新生血管、视网膜光凝和（或）冷凝治疗组与未治疗组之间VEGF和PDGF含量的比较分别采用方差分析、LsD-t检验和独立样本t检验,并对各组VEGF和PDGF含量进行Pearson相关分析.结果 NVG组房水中VEGF和PDGF含量分别为（926.3±223.5）ng/L和（226.2±81.5）ng/L,玻璃体液中分别为（1096.1±235.9）ng/L和（375.3±141.5）ng/L,均高于正常对照组（Z 房水VECG=-4.993,Z房水PDGF=-4.891,Z玻璃体VEGF=-4.991,Z玻璃体PDGF＝-4.992,P均=0.000）.不同原发病组比较：CRVO组房水和玻璃体液中VEGF含量均高于不明原凶组（t房水=1.746,P房水＝0.033;t玻璃体=1.917,P玻璃体=0.027）,其他各组之间VEGF含量差异均无统计学意义;DR组房水和玻璃体液中PDGF含量高于Eales病组（t房水=1.697,P房水：0.043;t玻璃体=1.762,P玻璃体=0.038）,其他各组间PDGF含量差异均无统计学意义.不同虹膜新牛血管分级组比较：各组房水和玻璃体液中VEGF含量差异均无统计学意义：虹膜新生血管Ⅳ级组玻璃体液中PDGF含量高于Ⅲ级组（t=1.740,P=0.049）.视网膜光凝和（或）冷凝治疗后,房水及玻璃体液中VEGF和PDGF的含量均低于未治疗组（Z房水VEGF＝2.945,P房水VEGF=0.003;t房水PDGF＝3.199,P房水PDGF＝0.002;Z玻璃体VEGF=3.165,P玻璃体VEGF＝002;t玻璃体PDGF＝2.984,P玻璃体PDGF＝0.004）.相关分析显示：NVG组房水中VEGF和PDGF含量呈正相关（r=0.305,P=0.025）,玻璃体液中VEGF和PDGF含量也呈正相关（r=0.303,P＝0.026）;CRVO组玻璃体液中VEGF和PDGF含量呈正相关（r=0.503,P＝0.040）;DR组房水中VEGF和PDGF含量呈正相关（r=0.462,P=0.030）.结论 NVG中VEGF和PDGF含量的变化与其原发病、虹膜新生血管严重程度有关,视网膜光凝和（或）冷凝治疗可抑制VEGF和PDGF的产生.     

糖尿病视网膜病变血浆与眼内液血管内皮生长因子的相关研究

目的　通过检测糖尿病性视网膜病变 (DR)患者血浆、眼内液 (房水、玻璃体 )血管内皮生长因子 (VEGF)含量 ,探讨其在 DR发展变化中的作用。　方法　采用双抗体夹心酶联免疫吸附试验 EL ISA法定量检测患者组及对照组血浆、房水、玻璃体 VEGF含量。　结果　无糖尿病性视网膜病变 (NDR)组血浆 VEGF含量 (34.4 7± 1.76 ) pg/ ml ,单纯型糖尿病性视网膜病变 (BDR)组血浆 VEGF含量 (5 3.93±3.0 8) pg/ ml,增生型糖尿病性视网膜病变 (PDR)组血浆 VEGF含量 (5 3.36± 3.2 8) pg/ ml,对照组血浆VEGF含量 (178.30± 10 .13) pg/ ml,与实验组比较差异均有显著性的意义 (P<0 .0 5 ) ;PDR组房水 VEGF含量 (184 .86± 12 .6 0 ) pg/ ml,对照组房水 VEGF含量 (90 .0 6± 18.32 ) pg/ ml,两者比较差异有显著性的意义 (P<0 .0 5 ) ;PDR组玻璃体 VEGF含量 (74 1.70± 92 .0 2 ) pg/ ml,对照组玻璃体 VEGF含量 (94 .38±2 1.2 1) pg/ ml,两者比较差异有显著性的意义 (P<0 .0 5 )。 PDR组血浆 VEGF与房水、玻璃体 VEGF无相关关系 (P>0 .0 5 ) ,玻璃体 VEGF与糖化血红蛋白 (Hb A1c)有正相关关系 (r=0 .90 6 7,P<0 .0 1)。　结论　糖尿病患者血浆 VEGF含量较正常人低 ,但与房水、玻璃体 VEGF含量无关 ;增生型糖尿病性视网膜病     

新生血管性青光眼患者眼内液血管 内皮生长因子的检测

目的了解新生血管性青光眼(neovascular glaucoma, NVG)患者房水及玻璃体中血管内皮生长因子(vascular endothelial growth factor, VEGF)的含量以及对虹膜新生血管发生的影响。方法应用酶联免疫吸附测定法(enzyme linked immu nosorbent assay, ELISA)分别对11例NVG患者行内眼手术时抽取的房水、玻璃体22个标本以及同期6例黄斑裂孔手术患者(对照组)房水、玻璃体12个标本进行VEGF检测。结果NVG患者房水、玻璃体中VEGF含量分别为(1.451±0.247)、(1.610±0.125) ng/ml,较对照组房水、玻璃体中的 VEGF含量(0.189±0.038)、(0.201±0.055) ng/ml明显增高, 两组间差别有非常显著性意义(t=12.007,P<0.001;t=26.057,P<0.001)。结论NVG患者房水、玻璃体中VEGF浓度显著增高,提示VEGF在NVG患者虹膜新生血管形成过程中可能具有一定作用。(中华眼底病杂志,2001,17:305-306)     

PDR患者玻璃体手术前后房水中VEGF水平的变化

目的：检测增殖性糖尿病视网膜病变(proliferative diabetic retinopathy,PDR)患者玻璃体手术前后房水中血管内皮生长因子(vascular endothelial growth factor, VEGF)的浓度变化,研究VEGF在PDR发病机制中的作用。

方法：收集30例PDR患者玻璃体手术前后的房水标本,以30例无糖尿病的白内障患者作为正常对照组,用酶联免疫吸附分析(enzyme-linked immunosorbent assay, ELISA)方法检测VEGF的浓度。

结果：PDR患者与正常对照组相比,房水中VEGF浓度显著升高,有统计学差异(P<0.05)。PDR患者玻璃体视网膜手术后与手术前相比,房水中VEGF浓度显著降低,有统计学差异(P<0.05)。

结论：VEGF积极参与了PDR的发生发展,并与PDR后期新生血管形成有着密切的关系。     

VEGF、IL-6的水平与糖尿病视网膜病变关系的研究

目的:检测2型糖尿病患者眼房水中血管内皮生长因子(Vascular endothelial growth factor,VEGF)和白细胞介素-6(Interleukin-6,IL-6)的含量,并探讨其临床意义.方法:在白内障手术过程中获取66例2型糖尿病患者的房水,采用双抗体夹心酶联免疫吸附(ELISA)法测定VEGF和IL-6的含量.根据手术后散瞳眼底检查和眼底荧光素血管造影检查确定糖尿病视网膜病变的分期.实验组分为:无糖尿病视网膜病变组(NDR)21例、单纯型糖尿病性视网膜病变组(BDR)26例、增生型糖尿病性视网膜病变组(PDR)19例,正常对照组为健康的老年性白内障患者20例.结果:NDR组、BDR组、PDR组的房水VEGF含量分别为(240.30±26.15)pg/ml、(292.27±58.91)pg/ml、(477.41±91.01)pg/ml,IL-6含量分别为(160.83±33.41)pg/ml、(238.60±62.23)pg/ml、(389.13±90.35)pg/ml,对照组房水VEGF含量为(140.58±26.27)pg/ml、IL-6含量为(82.72±21.53)pg/ml,对照组与实验组比较差异均有统计学意义(F=113.67,P＜0.01;F=106.53,P＜0.01).实验组房水中的VEGF与IL-6含量有相关性(r=0.995,P＜0.01);糖尿病患者的病程与房水中VEGF(r=0.792,0.826,0.841均P＜0.01)、IL-6(r=0.829,0.817,0.896均P＜0.01)含量有相关性.结论:VEGF、IL-6在糖尿病视网膜病变的形成过程中有重要作用,且两者之间有相关性.     

视网膜静脉阻塞和Eales病患者玻璃体内皮生长因子含量测定

目的：了解血管内皮生长因子(vascular endothelial growth factor，VEGF)在视网膜血管增殖性疾病患者玻璃体中的含量。 方法：采用酶联免疫吸附实验(enzyme linked immunosorbent assay，ELISA)测定伴有新生血管的视网膜静脉阻塞(retinal vein occlusion，RVO)和视网膜静脉周围炎(Eales病)患者玻璃体VEGF含量。 结果：RVO患者(7例)和Eales病患者(7例)玻璃体VEGF含量分别为(4.67士3.38)ng/ml和(1.79土0.44)ng/ml，是正常人(0.35土0.15)ng/ml的13倍和5倍(P<0.01)。 结论；RVO和Eales病患者玻璃体VEGF水平明显升高，提示VEGF可能参与其眼内新生血管增殖机制。 （中华眼底病杂志，1997，13：171-173）     

增生性糖尿病视网膜病变和增生性玻璃体视网膜病变患者玻璃体中TGF-β2的表达及意义

Objective To observe the expression of transforming growth factor-β2 （TGF-β2） in the vitreous body of patients with proliferative vitreoretinal diseases; to investigate the role of TGF-β2 in the pathogenesis of proliferative vitreoretinal diseases. Methods In an experimental study, vitreous specimens were obtained during vitrectomy from 61 patients （61 eyes） with proliferative vitreoretinal diseases. The vitreous specimens were obtained from 37 eyes with proliferative diabetic retinopathy （PDR） and 24 eyes with proliferative vitreoretinopathy （PVR）. Eight vitreous fluid samples were obtained from a normal control group. The concentrations of TGF-β2 in the vitreous body were detected by enzyme-linked immunosorbent assay （ELISA）. Results The concentrations of TGF-β2 in the vitreous bodies of eyes with PDR, PVR and the normal controls were 22.71±2.32 ng/ml, 21.28±1.7）ng/ml, and 19.00±0.62 ng/ml, respectively. Intravitreous concentrations of TGF-β2 were higher in patients with PDR and PVR than in the control group. The difference was statistically significant（F=7.756, P<0.01）. The concentration of TGF-β2 in the vitreous body from eyes of PDR patients was clearly higher than concentrations in PVR patients. The difference was statistically significant （P<0.05）. The concentrations of TGF-β2 in the vitreous body were higher in level Ⅵ of the PDR group in comparison to level Ⅴ of the PDR group. The difference was statistically significant （P<0.01）. The concentrations of TGF-β2 in the vitreous body were higher in the D class of the PVR group in comparison to the C class. The difference was statistically significant （P<0.01）. The concentrations of TGF-β2 in the vitreous bodies were positively correlated with the duration of the diseases： the correlation for the PDR group was r=0.705 （P<0.01） and the correlation for the PVR group was r=0.934（P<0.01）. Conclusion TGF-β2 may play an important role in the pathogenesis and development of proliferative vitreoretinal diseases.     

瘦素在增殖性糖尿病性视网膜病变和增殖性玻璃体视网膜病变中的表达

目的 通过检测瘦素在增殖性糖尿病性视网膜病变（proliferative diabetic retinopathy,PDR）和增殖性玻璃体视网膜病变（proliferative vitreous retinopathy,PVR）中的表达,探讨瘦素在PDR、PVR发生、发展过程中可能的调节机制。方法 分别用免疫组织化学染色的方法和酶联免疫吸附实验检测30例PDR患者、20例PVR病变患者眼内视网膜前膜中瘦素的表达,以及患者的血清、眼前房水、玻璃体液中瘦素的浓度。用Chi－Square Tests统计学方法分析和比较PDR、PVR与对照组之间瘦素表达的差异。结果 免疫组织化学染色结果：30例PDR患者中,有18例患者眼内视网膜前膜的瘦素受体呈阳性表达,阳性率为60%,与对照组比较,差异有统计学意义;20例PVR患者中,有3例患者眼内视网膜前膜的瘦素受体呈阳性表达,其中2例为血管纤维性视网膜前膜,1例为细胞纤维性视网膜前膜,阳性率为15%,与对照组比较,差异无统计学意义。ELISA结果：检测30例PDR患者的血清、眼前房水、玻璃体液中瘦素的浓度,与对照组之间差异有统计学意义（P＜0.05）;检测20例PVR患者的血清、眼前房水、玻璃体液中瘦素的浓度,与对照组之间差异无统计学意义（P＞0.05）。结论 瘦素可能主要是通过促进新生血管的生成参与到增殖性糖尿病性视网膜病变的发生、发展中,与增殖性玻璃体视网膜病变的发生、发展无明显相关性。     

抗VEGF辅助PPV治疗增生性糖尿病视网膜病变的效果及作用机制分析

目的:探讨抗血管内皮生长因子(vascular endothelial growth factor,VEGF)辅助玻璃体切割术(pars plana vitrectomy,PPV)治疗增生性糖尿病视网膜病变(proliferative diabetic retinopathy,PDR)的效果及作用机制.方法:将92例92眼行PPV的PDR患者,根据术前有无玻璃体腔注射雷珠单抗(intravitreal ranibizumab,IVR)分为单纯PPV组(41例41眼)和联合治疗组(51例51眼),其中联合治疗组于PPV术前5~7 d进行IVR.比较两组手术时间、电凝次数、硅油填充率、术后并发症发生率、术后3 mo患眼BCVA及手术前后不同时间点房水和玻璃体VEGF、色素上皮衍生因子(pigment epithelium-derived factor,PEDF)含量.结果:联合治疗组手术时间短于单纯PPV组,电凝次数少于PPV组,硅油填充、医源性视网膜裂孔及玻璃体再积血的几率均低于单纯PPV组,差异均有统计学意义(P<0.05);联合治疗组PPV时房水及玻璃体VEGF、PEDF含量低于单纯PPV组,差异均有统计学意义(P<0.05);联合治疗组术后3 mo患眼BCVA好于单纯PPV组,差异有统计学意义(P<0.05).结论:IVR联合PPV治疗PDR可降低PPV围手术期VEGF、PEDF水平,减少术中电凝次数,降低术后医源性视网膜裂孔及玻璃体再积血发生率,提高视力水平.     

增生性玻璃体视网膜疾病患者玻璃体中缺氧诱导因子-1α的表达及意义

背景增生性玻璃体视网膜疾病包括所有眼内过度增生性病变,许多细胞因子在其发病中起重要作用。缺氧诱导因子-1α（HIF-1α）参与多种缺血性疾病的发生发展,但是否在增生性玻璃体视网膜病变（PVR）发病中起作用尚不清楚。目的检测增生性玻璃体视网膜疾病患者玻璃体中HIF-1α的质量浓度,探讨HIF-1α在增生性玻璃体视网膜疾病发病中的作用。方法在常规玻璃体切割术中收集玻璃体标本,实验组共69例71眼,其中包括增生型糖尿病视网膜病变（PDR）患者37例39眼,PVR患者32例32眼;病例对照组16例16眼,其中包括黄斑裂孔（MH）14例14眼,黄斑前膜（ERM）2例2眼;正常对照组8例8眼。采用酶联免疫吸附测定法（ELISA）检测受检眼玻璃体中HIF-1α的质量浓度。结果实验组、病例对照组及正常对照组玻璃体中HIF-1α质量浓度分别为（294．08±2．97）、（260．41±8．29）、（16．38±3．56）mg／L,3组玻璃体中HIF-1α质量浓度比较差异有统计学意义（F=248．77,P=0．00）,其中实验组玻璃体中HIF-1α质量浓度高于正常对照组及病例对照组,差异有统计学意义（t=22．25,P=0．00;t=2．70,P=0．00）,病例对照组玻璃体中HIF-1α质量浓度高于正常对照组,差异有统计学意义（t=14．21,P=0．00）,PVR患者玻璃体中HIF-1α质量浓度与眼病史之间关联性较弱。结论增生性玻璃体视网膜疾病患者玻璃体中HIF-1α质量浓度增高,但与眼病史关联性较弱,HIF-1α可能在增生性玻璃体视网膜疾病发病中起一定作用。     

Cytokines in the vitreous fluid of patients with proliferative diabetic retinopathy--vascular endothelial growth factor and platelet-derived growth factor are elevated in proliferative diabetic retinopathy]

PURPOSE: To determine the relation between vascular endothelial growth factor (VEGF) and platlet-derived growth factor (PDGF) in the vitreous fluids from patients with proliferative diabetic retinopathy (PDR). SUBJECTS AND METHOD: Concentrations of VEGF and PDGF in the vitreous fluids from 53 eyes, 31 eyes in 30 PDR patients and 22 eyes in 22 non diabetes mellitus(DM) patients serving as controls, were measured by enzyme-linked immunosolvent assay. The levels of VEGF and PDGF were compared between PDR and non DM patients. The relationship between these factors and clinical characteristics such as age, sex, protein concentration in the aqueous humor, HbA1c and duration of diabetes were investigated. RESULTS: Levels of both VEGF and PDGF in the PDR group were significantly higher than in non DM group (p < 0.01). A positive correlation was observed between the levels of VEGF and protein concentration in the aqueous humor (p < 0.01). However, levels of both VEGF and PDGF did not correlate with age, sex, or HbA1c. CONCLUSION: Both VEGF and PDGF were shown to be correlated with the pathogenesis of PDR.     

Quantitative analysis of interleukin-6 in vitreous from patients with proliferative vitreoretinal diseases

PURPOSE: To explore immunological mechanisms in the pathogenesis of proliferative vitreoretinal diseases, we measured the concentration of interleukin-6 in the vitreous body and serum from patients with proliferative diabetic retinopathy (PDR), proliferative vitreoretinopathy (PVR), and premacular fibrosis. To evaluate immunological etiology, interleukin-6 levels in each disease were compared with disease severity. METHODS: Clinical samples were obtained at the beginning of pars plana vitrectomy from 30 eyes of 26 patients with PDR, 12 eyes of 12 patients with PVR, and 10 eyes of 10 patients with premacular fibrosis. Interleukin-6 was quantitated with an enzyme-linked immunosorbent assay. RESULTS: The levels of detectable interleukin-6 in the vitreous specimens ranged from 22.8 to 666.4 pg/mL in the PDR patients and from 28.2 to 416.3 pg/mL in the PVR patients. No interleukin-6 was detected in the vitreous specimens from patients with premacular fibrosis or in any serum samples from patients. Interleukin-6 levels of vitreous specimens from PDR patients were higher than those from PVR patients (P <.02, Mann-Whitney U-test). There was no correlation between clinical severity and interleukin-6 levels in vitreous specimens from either PDR or PVR patients. CONCLUSION: Our results indicated that cell-mediated immunity is involved in the pathogenesis of proliferative vitreoretinal diseases.     

Upregulation of RAGE and its ligands in proliferative retinal disease

We sought to study the presence of the receptor for advanced glycation endproducts (RAGE) and its ligands, advanced glycation endproducts (AGEs), S100/calgranulins and amphoterin (high mobility group box 1 protein; HMGB1), in the vitreous cavity and epiretinal membranes (ERMs) of eyes of patients with proliferative diabetic retinopathy (PDR) and proliferative vitreoretinopathy (PVR). Undiluted vitreous specimens were collected from 30 eyes of 30 patients undergoing pars plana vitrectomy for repair of retinal detachment (RD) secondary to PDR (n = 15) or PVR (n = 15). The vitreous samples obtained from 10 eyes undergoing macular hole repair were used as controls. Epiretinal membranes were obtained from eight eyes with PDR and from 10 eyes with PVR. The levels of AGEs in the vitreous were measured using ELISA. The vitreous levels of soluble RAGE (sRAGE), S100/calgranulins and amphoterin were measured using Western blot analyses. The localization of RAGE and its ligands in ERMs was determined with immunohistochemistry. The vitreous levels of sRAGE were significantly increased in both PDR and PVR (p < or = 0.05) compared to control vitreous. In both PDR and PVR, the vitreous levels of AGEs (p < or = 0.01), S100/calgranulins (p < or = 0.05), and amphoterin (p < or = 0.01) were also elevated compared to control eyes. Expression of RAGE was detected in six of eight ERMs from eyes with PDR and eight of 10 ERMs from eyes with PVR. Many cells expressing RAGE also expressed vimentin, suggesting a glial cell origin. Ligands for RAGE were also detected in ERMs, with AGEs detected in five eyes with PDR and eight eyes with PVR. Similarly, S100 and amphoterin ERM expression was observed in six eyes with PDR; these ligands were also expressed in ERMs from eyes with PVR (8 and 7 cases, respectively). We conclude that RAGE and its ligands are increased in the vitreous cavity of eyes with PDR and PVR and are present in ERMs of eyes with these proliferative retinal disorders. These findings suggest a role for the proinflammatory RAGE axis in the pathogenesis of proliferative retinal diseases.     

miRNA-15b和成纤维细胞生长因子2(FGF2)在增生型糖尿病视网膜病变患者玻璃体及视网膜增生膜组织中的表达

目的　探讨增生型糖尿病视网膜病变（PDR）患者玻璃体、视网膜增生膜组织中miRNA-15b（miR-15b）和成纤维细胞生长因子2（FGF2）的表达情况,并进行相关性研究,初步探讨PDR发生原因。方法　选取2016年9月至2019年10月期间在重庆市开州区人民医院眼科住院的PDR患者80例（80眼）作为PDR组,收集其玻璃体及视网膜增生膜组织;选取同期因眼外伤在本院眼科行眼球摘除术的2型糖尿病患者21例（21眼）作为对照组,收集其玻璃体及视网膜组织;通过实时荧光定量聚合酶链式反应（qRT-PCR）法检测玻璃体及视网膜组织/视网膜增生膜组织中miR-15b水平,分别通过酶联免疫吸附法（ELISA）、Western blot法检测玻璃体、视网膜组织/视网膜增生膜组织中FGF2蛋白水平表达;通过Pearson相关性分析法分析对照组玻璃体及视网膜组织以及PDR组患者玻璃体及视网膜增生膜组织中miR-15b与FGF2水平相关性;通过二元Logistic回归分析影响糖尿病患者发生PDR的危险因素。结果　PDR组糖尿病病程显著长于对照组（P<0.001）。PDR组玻璃体及视网膜增生膜组织中miR-15b相对表达量分别为0.52±0.07和0.76±0.12,均显著低于对照组（1.03±0.19和1.14±0.19）,差异均有统计学意义（均为P<0.001）;PDR组玻璃体及视网膜增生膜组织中FGF2蛋白表达水平分别为（17.65±4.23）ng·L^-1和0.92±0.23,均显著高于对照组［（12.13±3.05）ng·L^-1和0.61±0.15,均为P<0.001）］。对照组玻璃体、视网膜组织中miR-15b与FGF2蛋白表达水平均无相关性（均为P>0.05）;PDR组玻璃体、视网膜增生膜组织中miR-15b与FGF2蛋白表达水平均呈显著负相关（r=-0.708、-0.705,均为P<0.05）;二元Logistic回归分析结果显示,糖尿病病程长及玻璃体、视网膜增生膜组织中miR-15b水平低、FGF2蛋白表达水平高是影响糖尿病患者发生PDR的危险因素（均为P<0.01）。结论　玻璃体及视网膜增生膜组织中miR-15b与FGF2蛋白表达水平与PDR的发生密切相关。