天然抗氧化剂对糖尿病视网膜病变的预防和保护作用

氧化应激是糖尿病视网膜病变（diabetic retinopathy,DR）发生发展中常见的损伤机制,抗氧化剂作为氧化应激的抑制物在DR的预防与保护方面起一定的作用。天然抗氧化剂存在于植物或者食物中,具有易获取、患者易接受、副作用小以及部分可以通过饮食获取便可预防DR的进展等好处,成为目前应用抗氧化剂来预防及延缓DR研究的首选。多数抗氧化剂都可通过Nrf2信号通路发挥抗氧化作用,但信号通路上游及下游蛋白的复杂性导致其具体作用机制各不相同,因此各种抗氧化剂应用于DR的具体作用机制还有待进一步研究。（国际眼科纵览,2019, 43： 377-384）     

血红素氧合酶-1与糖尿病性视网膜病变:氧化应激的作用(英文)

糖尿病性视网膜病变(diabetic retinopathy,DR)是糖尿病最常见且严重的微血管并发症之一,其发病机制复杂,是多因素、多阶段作用的结果。近年研究表明,DR的发生与氧化应激密切相关,抗氧化治疗有助病情改善。血红素氧合酶-1(heme oxygenase-1,HO-1)是一种广泛存在的抗氧化防御酶,可对抗氧化应激造成的损伤,具有重要的生理作用。研究表明,在高血糖环境中,视网膜内HO-1的表达被诱导增高,且通过人为调节HO-1的表达水平可以加速或延缓病情的进展,提示将HO-1应用于DR的诊治有良好的应用前景。本文从氧化应激的角度对二者加以概述。     

复方血栓通胶囊对糖尿病大鼠视网膜氧化应激损伤保护作用的观察

糖尿病的并发症糖尿病视网膜病变(DR)严重影响患者生活质量,目前越来越多的证据显示氧化应激是DR发生与发展的关键机制~([1]).因此如果对糖尿病患者早期干预氧化应激损伤将起到预防或阻止视网膜病变发生发展的关键作用.本研究选用现代活血化瘀中药复方血栓通胶囊,现代药理研究证实该复方具有抗氧化、清除自由基、抗血小板、保护血管内皮细胞、降低血液黏度等作用~([2,3]).我们通过建立诱导的糖尿病大鼠模型,观察了复方血栓通胶囊对糖尿病大鼠视网膜氧化应激损伤保护作用.现将结果报道如下.     

细胞因子在糖尿病视网膜病变中的研究进展

糖尿病视网膜病变(diabetic retinopathy,DR)是糖尿病最严重和最常见的微血管并发症之一,也是一种世界范围内主要的致盲性眼病。其发病机制相当复杂,目前尚未完全明确。经典理论包括多元醇代谢异常、糖基化终产物的形成增加、蛋白激酶C的活化、氧化应激等。近年来,随着分子生物学的发展,分子基础研究已成为目前DR发病机制研究的焦点和热点。目前已知与DR有关的细胞因子有VEGF,IGF-1,bFGF,TNF等。多种细胞因子通过信号转导系统形成复杂的网络系统,引起新生血管生成,破坏血-视网膜屏障等多种改变,从而导致DR的发生发展。本文就细胞因子表达异常与DR的关系进行综述。     

褪黑素治疗糖尿病视网膜病变的研究进展

糖尿病视网膜病变(DR)是糖尿病在眼部的并发症之一,是工作人群视力下降的主要原因.DR的发病机制复杂,炎症、氧化应激、内质网应激和自噬等诸多因素均参与了DR的病理生理过程,目前尚缺乏有效的治疗措施.褪黑素是人脑松果体的合成产物,可释放到脑脊液和血液中;褪黑素及其代谢物具有多种生理功能,对炎症和氧化应激均具有拮抗作用.在...     

褪黑素对糖尿病视网膜病变防治作用的研究进展

大量的研究已经证实,氧化应激在糖尿病视网膜病变(DR)的发生中起主导作用.褪黑素(MLT)是体内很强的抗氧化剂之一,它可以直接清除体内自由基,或通过提高抗氧化酶的活性促进自由基的清除;MLT易于透过血-脑屏障抑制神经胶质细胞的反应性增生,防止视网膜神经组织的氧化损伤;MLT通过抑制诱导型一氧化氮合酶的表达,起到保护视网膜血管内皮细胞的作用;并具有调节血糖水平等作用.MLT针对DR的病因,从多方面起到防治DR的作用,有望成为主要的治疗药物.就近年来MLT对DR防治作用的研究进展做一综述.     

Nrf2通路在糖尿病视网膜病变中的研究进展

糖尿病视网膜病变(DR)作为糖尿病的一种严重并发症,可能导致严重的视力下降或丧失.核因子E2相关因子2(Nrf2)是一种在氧化应激及炎症相关组织损伤中发挥重要作用的氧化还原敏感转录因子.越来越多的研究表明,Nrf2在DR的发生和发展中起着重要作用.本文就Nrf2通路在糖尿病、DR发病中的作用及其与血管内皮生长因子(VEGF)表达的相关性进行综述.     

糖尿病视网膜病变相关“代谢记忆”的研究进展

糖尿病患者若高血糖不能及时有效控制，即使后期血糖长期控制良好，仍可能发生糖尿病慢性并发症即为高血糖的“代谢记忆”效应。糖尿病视网膜病变（DR）是糖尿病最常见的微血管并发症之一，糖尿病早期高血糖如不能得到及时控制，后期及时严格控制血糖，DR仍会发生、发展。多项糖尿病临床试验研究发现早期严格控制血糖可以延缓DR的病程，但糖尿病血管性应激物仍然处于高水平。炎症因子瀑布、氧化应激增强以及表观遗传修饰的变化等在高血糖“代谢记忆”现象发生发展中发挥重要作用。     

氧化应激在糖尿病视网膜病变中的作用及机制

糖尿病视网膜病变(Diabetic Retinopathy,DR)是临床上糖尿病患者出现的较为常见的并发症,也是糖尿病患者严重的微血管并发症之一糖尿病视网膜病变的发生原因较多,目前发病机制尚不明确,而氧化应激(OS)与DR的发生发展存在一定的相关性,参与并促进病变的发展.因此,本文对糖尿病视网膜病变氧化应激产生的原因与机制、氧化应激对视网膜组织的损伤机制等进行综述,以期更好的了解氧化应激与糖尿病视网膜病变的关系,为抗氧化疗法应用于糖尿病视网膜病变的治疗提供理论依据.     

血管生成促进因子在糖尿病视网膜病变新生血管形成中的作用

糖尿病视网膜病变(diabetic retinopathy,DR)是糖尿病最常见和最严重的并发症之一.目前,DR的发病机制尚不明确,但近年来研究表明,血管生成促进因子与DR新生血管的发生、发展密切相关,是导致视网膜新生血管形成的主要致病因子.本文就血管生成促进因子在DR新生血管形成中的作用进行综述.     

Analysis of a comprehensive diabetic retinopathy screening model for rural and urban diabetics in developing countries

AIM: To present an analysis of a screening model for diabetic retinopathy and compare the results of screening between rural and urban populations. METHODS: Between June 2003 and September 2004, 51 diabetic retinopathy screening camps (rural, 25; urban, 26) were conducted in three southern districts of India. The target population, aged 30 years and above, underwent comprehensive eye evaluation and those with referable diabetic retinopathy (proliferative diabetic retinopathy, severe non-proliferative diabetic retinopathy, severe diabetic macular oedema, or a combination of these) were referred to the base hospital for further treatment. RESULTS: Among 7716 diabetic subjects, the age and sex adjusted prevalence of diabetic retinopathy was 18% in the rural areas and 17% in the urban areas. The prevalence of referable retinopathy was 6.8% in rural areas and 4.6% in urban areas (p<0.001). Around 63% of individuals in rural areas and 75% in urban areas had never previously had their eyes examined for diabetic retinopathy. Multivariate analysis revealed the following risk factors for diabetic retinopathy: age more than 50 years, known diabetes, prolonged duration of diabetes, and eyes with moderate or severe visual impairment (p<0.0001). CONCLUSIONS: The study describes a comprehensive diabetic retinopathy screening model which can identify sight threatening retinopathy and provide necessary treatment for rural and urban populations.     

视网膜光凝治疗糖尿病性视网膜病变疗效观察

目的通过对糖尿病性视网膜病变(DR)行视网膜光凝治疗前后比较,评估视网膜光凝的治疗效果。方法回顾性比较分析87例(132只眼)糖尿病性视网膜病变行VISULAS 532 s激光局灶光凝或全视网膜光凝治疗前后的视力、眼底和荧光血管造影情况。结果平均随访时间14.8月。中度非增生性DR 32只眼光凝术前平均视力0.633,术后平均视力0.616,重度非增生性DR 83只眼术前平均视力0.316,术后平均视力0.278,增生性DR 17只眼术前平均视力0.145,术后平均视力0.116,均P>0.05。结论积极有效适度的视网膜光凝有利于稳定糖尿病性视网膜病变的视力和进展。     

Independence of retinopathy and optic atrophy in the DIDMOAD syndrome

A brother and a sister with DIDMOAD syndrome (diabetes insipidus, diabetes mellitus, optic atrophy, deafness, etc.) are described. The 15-year-old girl was suffering from severe optic atrophy, severe sensorineural hearing loss but only slight diabetic retinopathy. The 16-year-old boy presented with symptoms which were the opposite: slight optic atrophy, slight sensorineural hearing loss but severe diabetic retinopathy. These complementary impairments of neuronal and (diabetic) retinal function suggest that optic atrophy and retinopathy develop independently in DIDMOAD syndrome.     

Assessing the natural course of diabetic retinopathy: a population-based study in Kinmen, Taiwan

PURPOSE: To explore the natural course of diabetic retinopathy among type 2 diabetics using the indirect ophthalmoscope and single-field fundus photographs in Kinmen, Taiwan. METHODS: A screening program for diabetic retinopathy was carried out by a panel of ophthalmologists, who employed the ophthalmoscope and 45-degree retinal color photographs to examine the fundus after pupil dilation. Screening, which was conducted between 1999 and 2002, involved 971 patients diagnosed with type 2 diabetes. A multi-state Markov model was used to assess the natural course of diabetic retinopathy among type 2 diabetics. RESULTS: Among the 725 diabetes patients who attended at least two ophthalmological fundus check-ups and were screened, the overall response rate was about 75%. The mean duration of the disease states mild nonproliferative diabetic retinopathy, moderate nonproliferative diabetic retinopathy, severe nonproliferative diabetic retinopathy, and proliferative diabetic retinopathy were 4.05 [95% confidence interval (CI): 3.28-5.32], 4.18 (95% CI: 3.18-6.06), 2.52 (95% CI: 1.78-4.27), and 4.22 (95% CI: 2.88-7.81) years, respectively. Compared to controls, the incidence of blindness reduction for annual, biennial, 3-year, 4-year, and 5-year screenings of diabetic retinopathy were approximately 94.4% (95% CI: 91.6%-96.3%), 83.9% (95% CI: 83.6%-84.2%), 70.2% (95% CI: 69.8%-70.7%), 57.2% (95% CI: 56.7%-57.7%), and 45.6% (95% CI: 45.0%-46.1%), respectively. CONCLUSIONS: In conclusion, the average time for the development of diabetic retinopathy from nonexistence to blindness was approximately 26.5 years. The present recommendation for annual screening in type 2 diabetics with nonproliferative diabetic retinopathy should be retained only for the mild form, not for the moderate or severe forms.     

Evaluating the use of a scanning laser-derived oedema index to grade diabetic retinopathy and maculopathy

PURPOSE: To evaluate the Heidelburg Retina Tomograph II (HRTII) retinal module as a tool for grading severity of retinopathy in a diabetic retinal screening and treatment service. METHODS: Seventy-seven consecutive patients with type 2 diabetes underwent scanning laser tomography using the HRTII. Scan data were analysed using the proprietary macular module software and oedema indices calculated for each of nine topographic macular zones. Two consultant ophthalmologists, masked to the result of the HRTII scans, graded each subject for severity of retinopathy and presence of macular oedema. The oedema indices were analysed statistically to determine whether these correlated with severity of retinopathy and presence of macular oedema. RESULTS: There is an increased oedema index in severe non-proliferative diabetic retinopathy in the outer temporal zone compared with lesser grades of diabetic retinopathy (P = 0.001). In patients with clinically detectable macular oedema, the oedema index from the 500-microm-diameter central zone was significantly higher than those without (P = 0.03). CONCLUSION: The scanning laser-derived oedema index differentiated between moderate and severe non-proliferative diabetic retinopathy in this series and detected diabetic macular oedema. Further development of this technology may provide an important tool to supplement retinal photographic surveillance in eye clinics overwhelmed by an increasing prevalence of type 2 diabetes.     

Progression of diabetic retinopathy after pancreas transplantation. The University of Michigan Pancreas Transplant Evaluation Committee

The progression of diabetic retinopathy after combined pancreatic and kidney transplantation was studied in eight patients for 12 to 49 months. Four patients who had rapid pancreatic graft failure constituted a control group for comparison with four patients who retained functioning grafts. Using Fisher's exact probability test, the authors found no posttransplantation difference between the two groups in visual acuity lost, severity of diabetic macular edema, extent of capillary closure, progression of preretinal gliosis, development of disc or preretinal neovascularization, or worsening of the severity of the retinopathy. Achievement of normoglycemia by pancreatic transplantation is not effective in halting the progression of diabetic retinopathy in patients who already have severe diabetic microangiopathy joined the current follow-up.     

HLA antigens and other risk factors in the development of retinopathy in type 1 diabetes.

Factors possibly influencing the development of diabetic retinopathy were studied in 112 randomly selected type 1 diabetics having no or minimal retinopathy (group A) and in 82 type 1 diabetics with known severe diabetic retinopathy. The latter comprised those with severe background retinopathy (group B, n = 17) and those having proliferative retinopathy without (group C, n = 38) and with group D, n = 27) diabetic nephropathy. Nonretinopaths (group A) were of similar sex ratio, body weight, and age at diagnosis of diabetes but had been diabetic longer (p less than 0.001) and were thus older (p less than 0.001) than retinopaths (groups B-D). The distribution of HLA antigens of the A, B, and C loci was similar in nonretinopaths and retinopaths with the exception that HLA B7 showed a reduced (p less than 0.05) prevalence in the retinopaths (6% versus 17%) and was singularly underrepresented in group D, where no patients had this antigen. Mean postprandial plasma glucose and HbA1 concentrations were higher (p less than 0.01 and p less than 0.001) and cigarette smoking was more prevalent (p less than 0.01) in the retinopathy groups B-D than in group A. Systolic and diastolic blood pressures were similar in groups A-C, with higher (p less than 0.001) values only in group D. There was no association between insulin antibody binding in the serum or measurable plasma C-peptide immunoreactivity and retinopathy status. The risk of development of diabetic retinopathy in type 1 diabetes may be related to HLA-associated genetic factors and to cigarette smoking.     

Assessing the Natural Course of Diabetic Retinopathy: A Population-Based Study in Kinmen,Taiwan

Purpose: To explore the natural course of diabetic retinopathy among type 2 diabetics using the indirect ophthalmoscope and single-field fundus photographs in Kinmen, Taiwan. Methods: A screening program for diabetic retinopathy was carried out by a panel of ophthalmologists, who employed the ophthalmoscope and 45-degree retinal color photographs to examine the fundus after pupil dilation. Screening, which was conducted between 1999 and 2002, involved 971 patients diagnosed with type 2 diabetes. A multi-state Markov model was used to assess the natural course of diabetic retinopathy among type 2 diabetics. Results: Among the 725 diabetes patients who attended at least two ophthalmological fundus check-ups and were screened, the overall response rate was about 75%. The mean duration of the disease states mild nonproliferative diabetic retinopathy, moderate nonproliferative diabetic retinopathy, severe nonproliferative diabetic retinopathy, and proliferative diabetic retinopathy were 4.05 [95% confidence interval (CI): 3.28–5.32], 4.18 (95% CI: 3.18–6.06), 2.52 (95% CI: 1.78–4.27), and 4.22 (95% CI: 2.88–7.81) years, respectively. Compared to controls, the incidence of blindness reduction for annual, biennial, 3-year, 4-year, and 5-year screenings of diabetic retinopathy were approximately 94.4% (95% CI: 91.6%–96.3%), 83.9% (95% CI: 83.6%–84.2%), 70.2% (95% CI: 69.8%–70.7%), 57.2% (95% CI: 56.7%–57.7%), and 45.6% (95% CI: 45.0%–46.1%), respectively. Conclusions: In conclusion, the average time for the development of diabetic retinopathy from nonexistence to blindness was approximately 26.5 years. The present recommendation for annual screening in type 2 diabetics with nonproliferative diabetic retinopathy should be retained only for the mild form, not for the moderate or severe forms.     

Chirurgische Therapie der diabetischen Retinopathie und Makulopathie

Surgical therapy of diabetic retinopathy has been refined since the Early Treatment Diabetic Retinopathy Study (ETDRS). ETDRS did not perform panretinal photocoagulation at the time of surgery, which is currently considered a major part of vitrectomy, e.g., in vitreous hemorrhage. Despite improved surgical techniques, patient expectations and surgical outcome still differ considerably in severe cases of proliferative diabetic retinopathy. In this review of the literature we discuss the current surgical options and indications in diabetic retinopathy and maculopathy.     

The burgeoning public health impact of diabetes: the role of the ophthalmologist

With the recent increases and future projected increases in the incidence of type 2 diabetes mellitus and with the incidence increasing in teenagers and young adults, the already substantial public health effect of diabetes and diabetic retinopathy will become greater in years to come. Despite the strength of the evidence that optimizing control of glucose, blood pressure, and lipid levels will reduce the incidence and progression of diabetic retinopathy, metabolic control remains suboptimal for many patients with diabetes. In addition, many patients do not follow recommended guidelines for regular eye examinations, which is unfortunate because there is good evidence that with regular follow-up and intervention with photocoagulation as indicated, severe vision loss from diabetic retinopathy is uncommon. Yet, diabetic retinopathy is a leading cause of severe vision loss in adults. The current health care system too often fails to adequately manage diabetes and is lacking in providing proper education and motivation for patients to optimize their metabolic control. In addition to treating retinopathy, ophthalmologists can play an important role in educating and motivating patients to achieve better metabolic control, which, if successful, potentially could do more to reduce the progression of retinopathy than any of the ocular treatments currently in the armamentarium of the ophthalmologist.