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1.
糖尿病视网膜病变与细胞凋亡的研究近几年有许多相关文献发表,研究结果表明,糖尿病视网膜病变的发生发展与细胞凋亡有着密切的联系。在细胞凋亡方面的研究,大体可以分为内皮细胞、周细胞、神经细胞三大研究方面。细胞凋亡的研究为从根本上了解糖尿病视网膜病变的发病机制提供了新的思路及方法,为治疗糖尿病视网膜病变开辟了新的途径。  相似文献   

2.
目的观察醛糖还原酶抑制剂和肌醇对实验性糖尿病大鼠视网膜病变毛细血管周细胞的保护作用。方法给链脲佐菌素诱发的糖尿病大鼠分别管饲醛糖还原酶抑制剂或肌醇,于实验6个月末进行视网膜毛细血管消化铺片及透射电镜观察。结果糖尿病组的视网膜可见毛细血管内皮细胞/周细胞比值升高、无细胞毛细血管形成、周细胞线粒体肿胀、内皮细胞增生和毛细血管基底膜增厚;管饲醛糖还原酶抑制剂组的视网膜血管形态无明显改变;但管饲肌醇组的视网膜血管改变较管饲醛糖还原酶抑制剂组明显。结论醛糖还原酶抑制剂可有效预防实验性糖尿病性视网膜病变的形态学改变,肌醇能部分阻止视网膜形态学异常的发生。  相似文献   

3.
链脲佐菌素-糖尿病大鼠视网膜微血管病理改变   总被引:1,自引:1,他引:0  
目的:观察SIZ-糖尿病大鼠视网膜微血管的早期病理变化。方法:45只SD大鼠被随机分为糖尿病组(DM)和对照组(CON),用链脲佐菌素(streptozotocin,STZ)诱导SD大鼠建立糖尿病动物模型,分别饲养3个月和6个月。各组大鼠到期后,取眼球,采用视网膜消化铺片PAS染色、细胞图像分析及透射电镜技术进行早期糖尿病视网膜微血管形态学检查,记数微血管细胞数和无细胞血管数目,观察微血管及细胞超微结构。结果:糖尿病视网膜早期微血管周细胞数目逐渐减少,无细胞血管增多。超微结构显示微血管细胞结构异常,基底膜变性、增厚。结论:糖尿病视网膜病变早期存在微血管细胞病变、基底膜变性增厚及无细胞血管形成的改变。临床应重视糖尿病视网膜病变(DR)的早期防治,改善微血管循环。  相似文献   

4.
糖尿病视网膜病变最早期主要特征是基底膜增厚、内皮细胞紧密连接丧失、周细胞选择性丧失等微血管的形态改变,伴随血管渗透性增加、毛细血管闭塞、微动脉瘤,随后出现内皮细胞丧失.周细胞调节着血管张力和灌注压,周细胞凋亡会打破周细胞与内皮细胞之间的紧密联系,从而导致视网膜新生血管形成,这是临床上能最早观察到的糖尿病视网膜的血管异常.高血糖和局部血压增高是引起周细胞凋亡、丧失以及细胞内糖代谢异常的主要原因,然而具体机制尚未完全明确,需要进一步研究并寻找新的预防糖尿病视网膜病变的有效药物.  相似文献   

5.
糖尿病早期大鼠视网膜毛细血管细胞凋亡研究   总被引:14,自引:1,他引:13  
目的:研究早期糖尿病视网膜病变大鼠视网膜毛细血管细胞凋亡及其特征。方法:腹腔内注射链脲佐菌素诱导糖尿病大鼠模型。应用PAS染色、末端脱氧核苷酸转移酶介导的dUTP缺口标记(TUNEL)法标记和透镜观察进行研究。结果:在糖尿病3月和6月,可见周细胞和内皮细胞鬼影;周细胞和内皮细胞核异染色质聚集靠边并随病程进展而加重;被TUNEL法标记的细胞核染色质分布不均,表现为环形核、新月形核等。结论:早期糖尿病视网膜病变大鼠视网膜毛细血管周细胞丧失的性质为细胞凋亡,内皮细胞亦存在凋亡。  相似文献   

6.
目的:研究早期糖尿病视网膜病变的小鼠模型。方法:NOD小鼠随机分为正常对照组(4,12wk组,n=8)和糖尿病组(4,12wk组,n=12),每组取4wk和12wk处死小鼠,光镜和电镜观察视网膜结构的改变。结果:糖尿病组4wk时毛细血管基底膜增厚,可见内皮细胞、周细胞和神经节细胞超微结构改变。12wk时基底膜明显增厚,内皮细胞、周细胞和神经节细胞凋亡增加。结论:在糖尿病早期发生了视网膜神经元细胞超微结构病变和微血管病变。  相似文献   

7.
糖尿病性视网膜病变是糖尿病患者严重的眼部并发症,其病因和发病机制尚未阐明。近年来人们认为慢性高血糖引起体内糖基化蛋白的过量沉积,形成糖基化终产物,从而导致各系统的慢性疾病和功能丧失。传统上人们多认为糖尿病性视网膜病变主要是微血管病变,包括:内皮细胞增殖、基底膜增厚、周细胞丧失等。但目前许多临床研究表明:在糖尿病性视网膜病变微血管病变发生以前,糖尿病患者已有视功能改变。动物实验发现在糖尿病早期,  相似文献   

8.
糖尿病视网膜病变(diabetic retinopathy,DR)是导致视功能障碍和视力丧失的主要原因之一,其发病机制复杂,涉及多种细胞、分子,至今尚未完全阐明.DR的主要病理特点是微血管功能紊乱,其中周细胞凋亡是DR的重要标志.周细胞凋亡的主要原因包括高血糖引起的活性氧和糖基化终产物的产生增加,血小板衍生生长因子表达下降,血管生成素2和转化生长因子β的上调以及色素上皮衍生因子水平降低等.近年来,关于糖尿病视网膜微血管病变中周细胞分子调控机制的研究取得很大突破.因此,本文对DR中周细胞功能异常和其分子调控机制做一综述,为防治糖尿病视网膜微血管病变的发生提供新的理论基础.  相似文献   

9.
Tang J  An XL  Song HG  Bing H 《中华眼科杂志》2004,40(10):689-691
目的评价糖尿病患者视网膜组织学改变和细胞生化检测指标异常。方法将视网膜分为4个象限,胰酶消化法分离视网膜血管,比较各象限病变程度,将颞侧和鼻侧视网膜匀浆后检测其细胞生化指标。结果视网膜微动脉瘤、无细胞血管及凋亡周细胞的数量以颞侧多于鼻侧。视网膜各象限的糖转移因子、蛋白激酶C-β、半胱氨酸蛋白酶-1的检测结果明显不同。结论视网膜微血管病变和细胞生化检测指标异常程度在糖尿病视网膜病变患者视网膜的4个象限分布不均,推测其分布差异在糖尿病视网膜病变的发生、发展中起重要作用。(中华眼科杂志,2004,40:689-691)  相似文献   

10.
内皮素、一氧化氮与糖尿病视网膜病变   总被引:12,自引:0,他引:12  
内皮素和一氧化氮是两种作用相反的血管活性物质,两者共同作用影响眼底微循环血流动力学改变,与糖尿病视网膜病变中毛细血管的闭塞、内皮细胞的增殖、周细胞的凋亡以及基底膜的增厚密切相关,并对糖尿病视网膜病变的发病机制提出了新的认识,也为其治疗提供了新的思路。  相似文献   

11.
Diabetic retinopathy is the leading cause of blindness in the working age population. Unfortunately, there is no cure for this devastating ocular complication. The early stage of diabetic retinopathy is characterized by the loss of various cell types in the retina, namely endothelial cells and pericytes. As the disease progresses, vascular leakage, a clinical hallmark of diabetic retinopathy, becomes evident and may eventually lead to diabetic macular edema, the most common cause of vision loss in diabetic retinopathy. Substantial evidence indicates that the disruption of connexin-mediated cellular communication plays a critical role in the pathogenesis of diabetic retinopathy. Yet, it is unclear how altered communication via connexin channel mediated cell-to-cell and cell-to-extracellular microenvironment is linked to the development of diabetic retinopathy. Recent observations suggest the possibility that connexin hemichannels may play a role in the pathogenesis of diabetic retinopathy by allowing communication between cells and the microenvironment. Interestingly, recent studies suggest that connexin channels may be involved in regulating retinal vascular permeability. These cellular events are coordinated at least in part via connexin-mediated intercellular communication and the maintenance of retinal vascular homeostasis. This review highlights the effect of high glucose and diabetic condition on connexin channels and their impact on the development of diabetic retinopathy.  相似文献   

12.
The role of altered blood elements in the pathogenesis of retinal ischemia and diabetic retinopathy and the relationship to abnormal carbohydrate metabolism and to elevated levels of growth hormone are discussed. These changes involve red blood cells, platelets, plasma proteins, fibrinolytic response, and vascular endothelium. The significance of blood elements mediated by plasma is noted with aggregation of normal red cells when cross-matched with diabetic plasma and with intensive plasmapheresis, which caused red cell disaggregation and improvement of retinopathy. The relationship of metabolic control to diabetic retinopathy is reviewed and is evident by improvement of retinopathy occurring eight weeks after continuous subcutaneous infusion of insulin. A hypothesis is presented which integrates the multifactorial processes involved in the pathogenesis of diabetic retinopathy. Only through future research can one prove the implicated mechanisms in the pathogenesis of diabetic retinopathy and the role of strict metabolic control in altering the progression of retinopathy.  相似文献   

13.
杨曼  谭薇 《国际眼科杂志》2019,19(11):1874-1876

Müller细胞是脊椎动物视网膜最主要的神经胶质细胞,从内界膜到外界膜纵贯视网膜全层,参与构成血-视网膜屏障,积极参与视网膜发育并通过许多细胞内机制促进和维持视网膜稳态。Müller细胞在糖尿病视网膜病变的发生发展过程中扮演重要角色,其病理生理改变仍有待深入研究。本文就Müller细胞在糖尿病视网膜病变中的病理生理改变以及近年研究进展作一综述。  相似文献   


14.
On the pathogenesis of diabetic retinopathy   总被引:16,自引:0,他引:16  
R N Frank 《Ophthalmology》1984,91(6):626-634
Recent investigations of retinal vascular cells in tissue culture, animal models, and diabetic human subjects suggest several potential pathogenetic mechanisms for diabetic retinopathy. These include the enzyme aldose reductase, which appears to be responsible for basement membrane thickening in galactosemic rats (since the lesion is prevented by an aldose reductase inhibitor), and a picture, in galactosemic dogs, that closely resembles early, background diabetic retinopathy; insulin, which stimulates, and elevated glucose levels, which inhibit in vitro proliferation of retinal pericytes. Various hormones, including the sex hormone, the insulin-like growth factors and, perhaps independently, growth hormones, may influence the later stages of diabetic retinopathy. Chronic hyperglycemia appears to be the primary pathogenetic agent in diabetic retinopathy as well as in other complications of diabetes, but the different rates of onset and progression of these complications suggest that glucose acts through different biochemical pathways that are probably under different genetic control. Finally, the locus of the primary biochemical lesion in diabetic retinopathy may reside in the neuronal or glial cells of the retina, with the retinal blood vessels only secondarily involved.  相似文献   

15.
The most striking features of diabetic retinopathy are the vascular abnormalities that are apparent by fundus examination. There is also strong evidence that diabetes causes apoptosis of neural and vascular cells in the retina. Thus, there is good reason to define diabetic retinopathy as a form of chronic neurovascular degeneration. In keeping with the gradual onset of retinopathy in humans, the rate of cell loss in the animal models is insidious, even in uncontrolled diabetes. This is not surprising given that a sustained high rate of cell loss without regeneration would soon lead to catastrophic tissue destruction. The consequences of ongoing cell death are difficult to detect, and even the quantification of cumulative cell loss requires painstaking histology and microscopy. This subtle cell loss raises the issue of the relevance of the phenomenon to the progression of diabetic retinopathy and the ultimate loss of vision. Neuronal function may be compromised in advance of apoptosis, contributing to an early deterioration of vision. Here we review some of the evidence supporting apoptotic cell death as a contributing mechanism of diabetic retinopathy, explore some of the potential causes, and discuss the potential links between apoptosis and loss of visual function in diabetic retinopathy.  相似文献   

16.
Loss of blood-retinal barrier (BRB) integrity and vascular permeability characterizes diabetic retinopathy, and new therapies to reverse or prevent vascular permeability are needed to treat this debilitating disease. Glucocorticoids are currently under investigation for use as a local therapeutic treatment for diabetic retinopathy. This review examines the changes that occur to barrier properties in diabetic retinopathy and the potential to use glucocorticoids to restore vascular barrier properties in the retina. Glucocorticoids are useful in preserving the integrity of the blood-brain barrier in the treatment of brain tumors, and these steroids show similar effects on the retinal vasculature suggesting their potential usefulness in treating diabetic retinopathy. Recent progress has been made toward the goal of elucidating the precise mechanism underlying the protective effects of glucocorticoids on the retinal vasculature. Glucocorticoids may act by both suppressing inflammation and by directly affecting the endothelial cells by regulating phosphorylation, organization, and content of tight junction proteins. Further work will advance our understanding of glucocorticoid regulation of barrier properties allowing the ultimate goal of developing a specific and safe therapy to treat or prevent loss of the blood-neural barrier in a number of diseases, including brain tumors and diabetic retinopathy.  相似文献   

17.

外泌体是广泛存在于人体,由机体细胞产生并分泌的纳米级细胞外囊泡,能相对稳定地存在于各种生物组织和体液中,并携带特定的miRNA、蛋白质、转录因子等多种信息分子,参与调控体内多种疾病的病理生理过程。近年来随着外泌体在各学科研究的不断深入,其在眼科学领域的研究也迅速开展,目前发现外泌体在糖尿病视网膜病变、年龄相关性黄斑变性、自身免疫性葡萄膜炎、角膜病及青光眼等多种疾病中发挥重要作用。随着生活水平的提高,全世界糖尿病视网膜病变致盲人数逐年增加,而糖尿病视网膜病变机制研究未明,近年许多研究发现外泌体在其中发挥着重要作用,本文对外泌体在糖尿病视网膜病变的发生、发展机制的最新研究进展进行综述。  相似文献   


18.
Diabetic retinopathy is one of the most common devastating complications of diabetes. Pericyte loss, microaneurysms and acellular capillaries are characteristic for the diabetic retina. Researches have provided evidence that hyperglycaemia is one of the main factors driving the onset and progression of diabetic retinopathy. Although it has been shown that tight metabolic control has beneficial effects on the development and progression of this complication, the increase of blood glucose concentrations does not account for all the risk for development and progression to sight threatening retinopathy. A number of reports suggest that autoimmune mechanism play a role in diabetic microangiopathy (circulating antiendothelial cells autoantibodies, antiphospholipid antibodies, presence of immunoglobulins, lymphocytes and cytokines in diabetic retinal tissue). Diabetic subjects were also found to have autoantibodies to microvascular pericytes in their circulation. These results may contribute to understanding why retinopathy progresses in some patients, despite consistent reduction of blood sugar. This publication tries to estimate the anti-pericyte autoantibodies role in progression of diabetic retinopathy.  相似文献   

19.
目的:探讨非胰岛素依赖型糖尿病合并视网膜病变后其内皮细胞密度及形态学的变化。方法:选择40例糖尿病视网膜病变患者,分为增殖型视网膜病变组和非增殖型视网膜病变组。观察其内皮细胞密度及形态学变化,并与正常对照组进行比较,统计学分析。结果:糖尿病增殖型视网膜病变患者角膜内皮细胞密度及六边形细胞百分比明显降低,变异系数增加,糖尿病非增殖型视网膜病变患者角膜内皮细胞密度降低,形态学与下对照组比较差异无显著性。结论:非胰岛素依赖型糖尿病视网膜病变患者其角膜内皮细胞结构有异常变化。  相似文献   

20.
On the pathogenesis of diabetic retinopathy. A 1990 update   总被引:10,自引:0,他引:10  
R N Frank 《Ophthalmology》1991,98(5):586-593
Although most investigators now agree that chronic hyperglycemia is the basis for diabetic retinopathy, this has not been proven definitively. Even if chronic hyperglycemia is the initial common pathway leading to retinopathy and other complications of diabetes, it appears to act by different mechanisms in different tissues. The enzyme, aldose reductase, may play a major role in the development of diabetic retinopathy, but contradictory evidence exists. At the present time, results of the only study of aldose reductase inhibition and diabetic retinopathy reported in humans were negative. Another mechanism worthy of consideration is nonenzymatic glycation (glycosylation) of proteins, but there is no direct evidence of a causal role in diabetic retinopathy. Several growth factors have been identified in the retina that may promote neovascularization, and at least two inhibitors may prevent the process. There is evidence to support a role for basic and, perhaps, acidic fibroblast growth factors in retinal vasoproliferation. Transforming growth-factor beta, a peptide produced by capillary pericytes and smooth muscle cells and activated by the interaction of these cells with vascular endothelial cells, appears to be an important inhibitor of neovascularization, as is the vascular basement membrane.  相似文献   

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