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糖尿病视网膜病变患者血清内脂素水平变化与血管紧张素Ⅱ的关系

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中国误诊学杂志 2011年第34期11卷 8356-8356页

作者：张剑孙昊任永波徐志刚黑龙江佳木斯大学附属第一医院眼科 154003 淮安市第二人民医院

为探讨糖尿病视网膜病变患者血清内脂素（Visfatin）水平变化及与血管紧张素Ⅱ（AngⅡ）的关系,笔者测定了糖尿病患者血清内脂素、血浆AngⅡ水平,现报道如下。

关键词：糖尿病视网膜病变/代谢烟酰胺磷酸核糖基转移酶/代谢血管紧张素Ⅱ/代谢

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早期糖尿病大鼠视网膜谷氨酰胺合成酶的改变

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中华眼底病杂志 2007年第4期23卷 260-264页

作者：沈玺徐格致复旦大学附属眼耳鼻喉科医院眼科上海200031

目的：观察早期糖尿病大鼠视网膜谷氨酰胺合成酶（GS）的改变，探讨导致这种改变的发生机制。方法：链脲佐菌素（STZ）诱导糖尿病大鼠模型，采用间接免疫荧光组织化学法和Western蛋白印迹法检测1、2、3个月糖尿病大鼠组和对照组大鼠视网... 详细信息

目的：观察早期糖尿病大鼠视网膜谷氨酰胺合成酶（GS）的改变，探讨导致这种改变的发生机制。方法：链脲佐菌素（STZ）诱导糖尿病大鼠模型，采用间接免疫荧光组织化学法和Western蛋白印迹法检测1、2、3个月糖尿病大鼠组和对照组大鼠视网膜GS、白细胞介素-1β（IL-1β）和即早基因（c-Jun）的表达变化。另外分别将0、100、500、1000ng／ml IL-1β注入4组正常大鼠玻璃体腔中，24h后采用同样方法检测视网膜GS和c-Jun表达的变化。结果：对照组和1、2个月糖尿病大鼠组视网膜GS表达无明显改变，3个月糖尿病大鼠组GS表达与对照组相比明显下调（P〈0．01）；对照组中IL-1β、c-Jun只有极低表达，糖尿病大鼠1至3个月时IL-1β、c-Jun表达逐渐升高，与对照组相比差异有统计学意义（P〈0．01）。玻璃体腔注射500、1000ng／ml IL-1β可以使GS表达明显下调；注射100ng／ml IL-1β就可以使c-Jun表达显著升高，并呈剂量依赖性。结论：在早期糖尿病大鼠视网膜中，免疫相关因子IL-1β可使GS表达下降，其机制可能为IL-1β激活了c-Jun途径而影响GS的表达。

关键词：糖尿病视网膜病变/病因学糖尿病视网膜病变/代谢糖尿病视网膜病变/酶学谷氨酰胺连接酶/分析

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超氧化物歧化酶在视网膜毛细血管周细胞凋亡中的活性及意义

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眼科研究 2007年第5期25卷 321-324页

作者：陈百华龙剑锋姜德咏唐罗生中南大学湘雅二医院眼科长沙410011

目的通过检测糖基化终产物(AGE)诱导培养的牛视网膜毛细血管周细胞凋亡及凋亡周细胞中超氧化物歧化酶(SOD)的活性及意义,进一步探讨糖尿病视网膜病变(DR)的发生机制。方法周细胞分别与不同浓度的AGE(0.47、1.88、7.5μmol/L)共同培养4d... 详细信息

目的通过检测糖基化终产物(AGE)诱导培养的牛视网膜毛细血管周细胞凋亡及凋亡周细胞中超氧化物歧化酶(SOD)的活性及意义,进一步探讨糖尿病视网膜病变(DR)的发生机制。方法周细胞分别与不同浓度的AGE(0.47、1.88、7.5μmol/L)共同培养4d后,分别检测细胞凋亡、SOD活性,以及SOD对细胞凋亡及凋亡调节基因Bcl-2/Bax比率的影响。结果AGE能以浓度依赖的方式诱导周细胞凋亡(r=0.878,P<0.01)、降低细胞内SOD的活性(r=-0.878,P<0.01),而应用SOD能明显抑制AGE作用下的周细胞凋亡及提高凋亡调节基因Bcl-2/Bax的比率。结论凋亡及氧化应激的增加是DRP中周细胞选择性丧失的主要原因,SOD活性的下降是AGE诱导周细胞发生凋亡的关键因素。

关键词：周细胞/代谢糖基化终产物超氧化物歧化酶糖尿病视网膜病变/代谢

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AGEs及脂质代谢紊乱与糖尿病视网膜病变的关系

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吉林大学学报（医学版） 2005年第1期31卷 104-107页

作者：杨威宋鄂刘克辉吉林大学第一医院眼科吉林长春130021 吉林大学第一医院内分泌科吉林长春130021

目的 :探讨高级糖基化终末产物 (AGEs)及脂质代谢紊乱与糖尿病视网膜病变 (DR)的关系。方法 :对 35例 2型糖尿病并发 DR患者、 31例 2型糖尿病无 DR(NDR)患者及 16例正常人的血清 AGEs水平及脂质代谢各项指标进行检测。结果 :1DR组及 ND... 详细信息

目的 :探讨高级糖基化终末产物 (AGEs)及脂质代谢紊乱与糖尿病视网膜病变 (DR)的关系。方法 :对 35例 2型糖尿病并发 DR患者、 31例 2型糖尿病无 DR(NDR)患者及 16例正常人的血清 AGEs水平及脂质代谢各项指标进行检测。结果 :1DR组及 NDR组患者的血清 AGEs水平均较正常人显著升高 (P<0 .0 5 ) ,DR组患者的血清 AGEs水平较 NDR组增高 ,但差异无统计学意义 (P>0 .0 5 ) ;2 NDR组患者的血清低密度脂蛋白 (L DL- C)水平显著高于正常人 (P<0 .0 5 ) ,血清高密度脂蛋白 (HDL- C)、载脂蛋白 A1(APOA1)水平较正常人显著降低 (P<0 .0 5 ) ,DR组患者血清总胆固醇 (TCH)、甘油三脂 (TG)、 L DL- C水平均显著高于正常人(P<0 .0 5 ) ;3DR患者的血清 TCH、HDL- C及 L DL- C水平较 NDR组显著升高 (P<0 .0 5 ) ;4多因素线性相关分析显示血清 AGEs水平与血清 TCH、 TG、 APOB和 L DL- C水平呈正相关 (r值分别为 0 .70 5、 0 .5 1、 0 .6 0和0 .6 0 )。结论 :AGEs大量生成和堆积、脂质代谢紊乱及二者间的相互作用是 2型糖尿病患者并发 DR的重要危险因素 ,严格控制血糖的同时积极纠正脂质代谢紊乱 ,对于延缓和控制 DR的发生发展具有重要意义。

关键词：糖尿病视网膜病变/代谢糖基化终产物,高级/代谢脂质代谢紊乱

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Platelets accumulate in the diabetic retinal vasculature following endothelial death and suppress blood-retinal barrier breakdown

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AMERICAN JOURNAL OF PATHOLOGY 2003年第1期163卷 253-259页

作者： Yamashiro, K Tsujikawa, A Ishida, S Usui, T Kaji, Y Honda, Y Ogura, Y Adamis, AP Harvard Univ Massachusetts Eye & Ear Infirm Sch Med Angiogenesis Retina Res Lab Boston MA 02114 USA Kyoto Univ Grad Sch Med Dept Ophthalmol & Visual Sci Kyoto Japan Keio Univ Sch Med Dept Ophthalmol Tokyo Japan Univ Tokyo Fac Med Dept Ophthalmol Tokyo Japan Nagoya City Univ Sch Med Dept Ophthalmol Nagoya Aichi 467 Japan Eyetech Res Ctr Woburn MA 01801 USA

Platelet microthrombi are present in the diabetic retinal vasculature of humans and rodents;however, the mechanisms and consequences of their presence have not been defined. The current study demonstrates that platelet containing microthrombi accumulate in the retinal vasculature of the rat within 2 weeks of experimental diabetes, a timepoint at which leukocyte-mediated endothelial cell injury and death are known to occur. Platelet accumulation increased with the duration of diabetes, and crossover experiments revealed that maximal platelet accumulation required both diabetic platelets and a diabetic endothelium. Platelet accumulation also coincided with the expression of Fas and FasL in the diabetic retina. When endothelial cell apoptosis was inhibited with an anti-FasL neutralizing antibody, platelet accumulation was effectively suppressed. When platelets were depleted from the systemic circulation with an antiplatelet antibody, blood-retinal barrier breakdown worsened in the diabetic animals. These findings suggest that platelet accumulation in the diabetic retinal vasculature is secondary to endothelial cell death and serves, in part, to suppress blood-retinal barrier breakdown.

关键词：抗原 CD95/代谢血小板血视网膜屏障/生理学糖尿病实验性糖尿病视网膜病变/代谢糖尿病视网膜病变/病理学内皮血管/代谢内皮血管/病理学 Fas配体蛋白质膜糖蛋白类/代谢大鼠 Long-Evans 视网膜血管/代谢视网膜血管/病理学血栓形成时间因素动物人类男(雄)性大鼠

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Increased levels of vascular endothelial growth factor and interleukin-6 in the aqueous humor of diabetics with macular edema

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AMERICAN JOURNAL OF OPHTHALMOLOGY 2002年第1期133卷 70-77页

作者： Funatsu, H Yamashita, H Noma, H Mimura, T Yamashita, T Hori, S Tokyo Womens Med Univ Ctr Diabet Dept Ophthalmol Shinjuku Ku Tokyo 1628666 Japan Yamagata Univ Sch Med Dept Ophthalmol Yamagata 99023 Japan Hiroshima Univ Sch Med Dept Ophthalmol Hiroshima Japan

PURPOSE: To investigate the relationship between diabetic macular edema and the levels of vascular endo. thelial growth factor VEGF) and interleukin 6 (IL-6) in aqueous humor and plasma. DESIGN: Comparative cross-sectional study. METHODS: Fifty,four eyes from 54 diabetic patients were used. The concentrations of VEGF and IL-6 in undiluted aqueous specimens (obtained from the eyes during cataract surgery) and in plasma were measured by an enzyme-linked immunosorbent assay. To assess bloods aqueous barrier function, the aqueous flare intensity was measured by a laser flare,cell meter as an estimate of the aqueous protein level. RESULTS: The aqueous levels of VEGF and IL-6 were significantly correlated with the severity of macular edema (P = 0.628, P <.001 and p = 0.517, P <.01 respectively), as well as with the aqueous protein concentration (p = 0.618, P <.001 and p = 0.588, P <.001, respectively). Aqueous levels of VEGF and IL-6 were significantly higher than their respective plasma levels (both P <.001). In addition, the aqueous level of VEGF was significantly correlated with that of IL-6 (p = 0.537, P <.01). Furthermore, the status of the posterior vitreous significantly correlated with the severity of macular edema (1) = 0.618, P <.000 1). CONCLUSIONS: These results suggest that both VEGF and IL-6 are produced together in the intraocular tissues, and are involved in the pathogenesis of macular edema.

关键词：眼房水/代谢血房水屏障横断面研究糖尿病视网膜病变/分类糖尿病视网膜病变/并发症糖尿病视网膜病变/代谢内皮生长因子/代谢酶联免疫吸附测定眼蛋白质类/代谢白细胞介素6/代谢淋巴因子/代谢黄斑水肿/分类黄斑水肿/病因学黄斑水肿/代谢血管内皮生长因子A 血管内皮生长因子类成年人老年人女(雌)性人类男(雄)性中年人

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Retinal vascular endothelial growth factor induces intercellular adhesion molecule-1 and endothelial nitric oxide synthase expression and initiates early diabetic retinal leukocyte adhesion in vivo

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AMERICAN JOURNAL OF PATHOLOGY 2002年第2期160卷 501-509页

作者： Joussen, AM Poulaki, V Qin, WY Kirchhof, B Mitsiades, N Wiegand, SJ Rudge, J Yancopoulos, GD Adamis, AP Massachusetts Eye & Ear Infirm Boston MA 02114 USA Childrens Hosp Surg Res Lab Boston MA 02115 USA Dana Farber Canc Inst Boston MA 02115 USA Regeneron Pharmaceut Inc Tarrytown NY 10591 USA Univ Cologne Dept Vitreoretinal Surg Ctr Opthalmol Cologne Germany Univ Cologne Zentrum Mol Med Cologne Germany

Leukocyte adhesion to the diabetic retinal vasculature results in early blood-retinal barrier breakdown, capillary nonperfusion, and endothelial cell injury and death. Previous work has shown that intercellular adhesion molecule-1 (ICAM-1) and CD18 are required for these processes. However the relevant in vivo stimuli for ICAM-1 and CD18 expression in diabetes remain unknown. The current study investigated the causal role of endogenous vascular endothelial growth factor (VEGF) and nitric oxide in initiating these events. Diabetes was induced in Long-Evans rats with streptozotocin, resulting in a two- to threefold increase in retinal leukocyte adhesion. Confirmed diabetic animals were treated with a highly specific VEGF-neutralizing Flt-Fc construct (VEGF TrapA(40)). Retinal ICAM-1 mRNA levels in VEGF TrapA(40)-treated diabetic animals were reduced by 83.5% compared to diabetic controls (n = 5, P < 0.0001). VEGF TrapA40 also potently suppressed diabetic leukocyte adhesion in retinal arterioles (47%, n = 11, P < 0.0001), venules (36%, n = 11, P < 0.0005), and capillaries (36%, n = 11, P < 0.001). The expression of endothelial nitric oxide synthase (eNOS), a downstream mediator of VEGF activity, was increased in diabetic retina, and was potently suppressed with VEGF TrapA(40) treatment (n = 8 P < 0.005). Further, VEGF TrapA(40) reduced the diabetes-related nitric oxide increases in the retinae of diabetic animals. The inhibition of eNOS with N-ω-nitro-L-arginine methyl ester also potently reduced retinal leukocyte adhesion. Although neutrophil CD11a, CD11b, and CD18 levels were increased in 1-week diabetic animals, VEGF TrapA(40) did not alter the expression of these integrin adhesion molecules. Taken together, these data demonstrate that VEGF induces retinal ICAM-1 and eNOS expression and initiates early diabetic retinal leukocyte adhesion in vivo. The inhibition of VEGF bioactivity may prove useful in the treatment of the early diabetic retinopathy.

关键词：细胞黏附糖尿病实验性/代谢糖尿病实验性/病理生理学糖尿病视网膜病变/代谢糖尿病视网膜病变/病理生理学内皮生长因子/代谢酶抑制剂/药理学免疫组织化学整合素类/代谢胞间黏附分子1/遗传学胞间黏附分子1/代谢白细胞/代谢白细胞/生理学淋巴因子/代谢 NG-硝基精氨酸甲酯/药理学一氧化氮合酶/遗传学一氧化氮合酶/代谢一氧化氮合酶Ⅲ型亚硝酸盐类/代谢大鼠 Long-Evans 视网膜/酶学视网膜/代谢视网膜血管/生理学血管内皮生长因子A 血管内皮生长因子类动物男(雄)性大鼠

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Pigment epithelium-derived factor in the vitreous is low in diabetic retinopathy and high in rhegmatogenous retinal detachment

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AMERICAN JOURNAL OF OPHTHALMOLOGY 2001年第3期132卷 378-382页

作者： Ogata, N Tombran-Tink, J Nishikawa, M Nishimura, T Mitsuma, Y Sakamoto, T Matsumura, M Kansai Med Univ Dept Ophthalmol Osaka 5708507 Japan George Washington Univ Med Ctr Washington DC 20037 USA Univ Missouri Kansas City MO 64110 USA Kyushu Univ Dept Ophthalmol Fukuoka 812 Japan

PURPOSE: To report the levels of pigment epithelium-derived factor in the vitreous of patients with diabetic retinopathy, rhegmatogenous retinal detachment, and idiopathic macular hole. METHODS: Using enzyme,linked immunosorbent as, say, we measured the levels of pigment epithelium-derived factor in the vitreous of 34 eyes of 33 patients who underwent vitrectomy for the treatment of diabetic retinopathy (17 eyes of 16 patients), rhegmatogenous retinal detachment (10 eyes), and idiopathic macular hole (seven eyes). RESULTS: The vitreal concentration of pigment epithelium-derived factor was 1.15 +/- 0.23 mug/ml (mean +/- standard error) in eyes with diabetic retinopathy, 3.28 +/- 0.69 mug/ml in rhegmatogenous retinal detachment, and 1.71 +/- 0.39 mug/ml in idiopathic macular hole. The pigment epithelium-derived factor level in rhegmatogenous retinal detachment was significantly higher than that in diabetic retinopathy (P = .0008) and idiopathic macular hole (P = .034). For eyes with diabetic retinopathy, the pigment epithelium-derived factor level was 0.88 +/- 0.21 mug/ml in proliferative diabetic retinopathy and 2.43 +/- 0.37 mug/ml in nonproliferative diabetic retinopathy (P = .0083). Additionally, the pigment epithelium-derived factor level in active diabetic retinopathy (0.70 +/- 0.22 mug/ml) was significantly lower than the level in inactive diabetic retinopathy (1.79 +/- 0.35 mug/ml;P = .018). CONCLUSIONS: These results suggest that pigment epithelium-derived factor inhibits angiogenesis and that lower levels of pigment epithelium-derived factor may be related to the angiogenesis in diabetic retinopathy and result in active proliferative diabetic retinopathy. The results also suggest that higher levels of pigment epithelium-derived factor in the eyes with rhegmatogenous retinal detachment may act as a neuroprotective agent for the detached retina. (Am J Ophthalmol 2001;132: 378-382. (C) 2001 by Elsevier Science Inc. All rights reserved.).

关键词：糖尿病视网膜病变/代谢糖尿病视网膜病变/外科学酶联免疫吸附测定眼蛋白质类/代谢神经生长因子类蛋白质类/代谢视网膜脱离/代谢视网膜脱离/外科学视网膜穿孔/代谢视网膜穿孔/外科学舍平类/代谢玻璃体切除术玻璃体/代谢成年人老年人女(雌)性人类男(雄)性中年人

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Vitrectomy for diabetic macular edema: The role of posterior vitreous detachment and epimacular membrane

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AMERICAN JOURNAL OF OPHTHALMOLOGY 2001年第3期132卷 369-377页

作者： Yamamoto, T Akabane, N Takeuchi, S Toho Univ Sakura Hosp Dept Ophthalmol Chiba 2858741 Japan

PURPOSE: To evaluate the surgical efficacy of pars plana vitrectomy on eyes with diabetic macular edema in the presence or absence of a complete posterior vitreous detachment and with or without an epimacular membrane. METHODS: Pars plana vitrectomy was performed on 30 eyes of 29 cases with diabetic macular edema. Visual acuity was measured, and retinal thickness was determined by optical coherence tomography before and after vitrectomy. To evaluate the relationship between the effects of vitrectomy and the presence or absence of posterior vitreous detachment and/or epimacular membrane, all eyes were placed into one of four groups: group A, eyes with posterior vitreous detachment and epimacular membrane;B, eyes with posterior vitreous detachment and without epimacular membrane;C, eyes without posterior vitreous detachment and with epimacular membrane;and D, eyes without posterior vitreous detach, ment and without epimacular membrane. The expression of vascular endothelial growth factor and interleukin-6 was investigated immunohistochemically in epimacular membrane specimens obtained from seven eyes with diffuse diabetic macular edema. RESULTS: The postoperative mean visual acuity (0.653 +/- 0.350: mean +/- SD logarithm of minimal angle of resolution [logMAR]) was significantly better than the mean preoperative visual acuity (0.891 +/- 0.319 log-MAR;Wilcoxon signed-rank test, P = .0007). The postoperative foveal thickness (264.5 +/- 118.6 mum) was significantly thinner than the preoperative foveal thick, ness (477.8 +/- 147.7 mum;Wilcoxon signed,rank test, P < .0001). There were no significant differences in the improvement of visual acuity and decrease of foveal thickness between the four groups (Kruskal-Wallis test, P = .13, P = .65, respectively). All of the epimacular membranes obtained at surgery expressed vascular endothelial growth factor and interleukin-6. CONCLUSIONS: These results demonstrated that vitrectomy with removal of epimacular membrane is generally

关键词：糖尿病视网膜病变/代谢糖尿病视网膜病变/病理学糖尿病视网膜病变/外科学内皮生长因子/代谢视网膜外膜/代谢视网膜外膜/病理学视网膜外膜/外科学免疫酶技术白细胞介素6/代谢淋巴因子/代谢回顾性研究血管内皮生长因子A 血管内皮生长因子类视敏度玻璃体切除术玻璃体脱离/代谢玻璃体脱离/病理学玻璃体脱离/外科学老年人女(雌)性人类男(雄)性中年人

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Bax is increased in the retina of diabetic subjects and is associated with pericyte apoptosis in vivo and in vitro

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AMERICAN JOURNAL OF PATHOLOGY 2000年第3期156卷 1025-1032页

作者： Podestà, F Romeo, G Liu, WH Krajewski, S Reed, JC Gerhardinger, C Lorenzi, M Harvard Univ Sch Med Schepens Eye Res Inst Boston MA 02114 USA Harvard Univ Sch Med Dept Ophthalmol Boston MA 02114 USA Burnham Inst La Jolla CA 92037 USA

Diabetes of even short duration accelerates the death of capillary cells and neurons in the inner retina by a process consistent with apoptosis. We examined whether the process is accompanied by changes in the expression of endogenous regulators of apoptosis. In postmortem retinas of 18 diabetic donors (age 67 +/- 6 years, diabetes duration 9 +/- 4 years) the levels of pro-apoptotic Bax were slightly, but significantly, increased when compared with levels in 20 age-matched nondiabetic donors (P = 0.04). In both groups, Bax localized to vascular and neural cells of the inner retina. Neither pro-apoptotic Bcl-X-S, nor pro-survival Bcl-X-L appeared affected by diabetes. The levels of these molecules could not be accurately quantitated in lysates of retinal vessels because of variable degrees of glial contamination. However, studies in situ showed in several pericytes, the outer cells of retinal capillaries, intense Bax staining often in conjunction with DNA fragmentation. Bovine retinal pericytes exposed in vitro to high glucose levels for 5 weeks showed elevated levels of Bax (P = 0.03) and increased frequency of annexin V binding, indicative of early apoptosis, Hence, human diabetes selectively alters the expression of Bax in the retina and retinal vascular pericytes at the same time as it causes increased rates of apoptosis. The identical program induced by high glucose in vitro implicates hyperglycemia as a causative factor in vivo, and provides a model for establishing the role of Bax in the accelerated death of retinal cells induced by diabetes.

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