Treatment of Diabetic Retionpathy by Inhibition of Adhesion Molecules

通过抑制粘附分子治疗糖尿病视网膜病变

• 批准号: 13671832
• 负责人: KIRYU Junichi
• 金额: $ 2.56万
• 依托单位: KYOTO UNIVERSITY
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2001
• 资助国家: 日本
• 起止时间: 2001 至 2002
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-13671832/
• 关键词: diabetes; retina; leukocyte; 細膜虚血; precouditioning; 白血球・血管内皮相互作用; Acridine Orange Disital Flourography; adenosine Al受容体; 糖尿病網膜症; 網膜光凝固; 血管透過性

In diabetic retinopathy, leukocyte accumulation is elevated by the stimulation of leukocyte-endothelial cell interactions. The accumulated leukocytes injure the vascular endothelial cells and leads to the blood-retinal barrier breakdown. The leukocyte-endothelial cell interactions are regulated by adhesion molecules, such as P-selection or ICAM (intracellular adhesion molecule)-1. Antithrombin III and histamine H1 receptor antagonist inhibited the expression of adhesion molecules and leukocyte-endothelial interactions. These results suggest that these drugs may have same effects in diabetic retinopathyPlatelet-endothelial cell interactions in the retinal microcirculation are quantitatively evaluated. This method is valuable because these interactions stimulate leukocyte-endothelial cell interactions in addition to platelet activationMoreover, the inflammatory response after scatter laser photocoagulation in retina was evaluated. The scatter laser photocoagulation is a major treatment for diabetic retinopathy and inflammatory reactions are one of the severe complications. Leukocyte-endothelial interactions play an important role in this model and it may be useful to inhibit the interactions to treat the inflammation after laser treatment in diabetic retinopathy

在糖尿病性视网膜病变中，白细胞积聚通过白细胞-内皮细胞相互作用的刺激而升高。积聚的白细胞损伤血管内皮细胞并导致血-视网膜屏障破坏。白细胞与内皮细胞的相互作用受粘附分子如P-选择素或ICAM-1的调节。抗凝血酶III和组胺H1受体拮抗剂抑制粘附分子的表达和白细胞-内皮细胞相互作用。这些结果表明，这些药物可能对糖尿病视网膜病变具有相同的作用。这种方法是有价值的，因为这些相互作用刺激白细胞-内皮细胞的相互作用，除了血小板活化。此外，散射激光光凝后的视网膜炎症反应进行了评估。散射激光光凝是治疗糖尿病视网膜病变的主要方法，炎症反应是其严重并发症之一。白细胞-内皮细胞相互作用在该模型中起重要作用，抑制白细胞-内皮细胞相互作用可能有助于治疗糖尿病视网膜病变激光治疗后的炎症反应

项目成果

野中 淳之: "Inflammatory response after scatter laser photocoagulation in nonphotocoagulated retina"Investigative Ophthalmology and Visual Science. 43・4. 1204-1209 (2002)

Atsuyuki Nonaka：“非光凝视网膜中散射激光光凝后的炎症反应”调查眼科和视觉科学 43・4（2002 年）。

Nishijima K, Kiryu J, Tsujikawa A, Honjo M, Nonaka A, Yamashiro K, Tanihara H, Tojo SJ, Ogura Y, Honda Y: "In vivo evaluation of platelet-endotheliaJ interactions after transient retinal ischemia"Invest Ophthalmol Vis Sci. 42(9). 2102-2109 (2001)

Nishijima K、Kiryu J、Tsujikawa A、Honjo M、Nonaka A、Yamashiro K、Tanihara H、Tojo SJ、Ogura Y、Honda Y：“短暂性视网膜缺血后血小板-内皮细胞相互作用的体内评估”Invest Ophasemol Vis Sci。

野中淳之: "Inhibitory Effect of Ischemic Preconditioning on Leukocyte participation in Retinal Ischemia-Reperfusion Injury"Investigative Ophthelurology & Visual Science. 42. 2380-2385 (2001)

Atsuyuki Nonaka：“缺血预处理对白细胞参与视网膜缺血再灌注损伤的抑制作用”调查眼科与视觉科学 42. 2380-2385 (2001)。

山城 健児 他: "Inhibitory effects of antithrombin III against leukocyte rolling and infrltration during endotoxin-induced weitis in rats"Inrestigative Opthalmology and Visual Science. 42・7. 1553-1560 (2001)

Kenji Yamashiro 等人：“抗凝血酶 III 对大鼠内毒素诱导的尿炎期间白细胞滚动和浸润的抑制作用”Inrestigative Opthalmology and Visual Science 42・7 (2001)。

山城 健児 他: "Suppressive effects of histamine H1 receptor antagonist diphendydramine on the leukocyte infiltration during endotoxin-induced uveitis"Experimental Eye Research. 73・1. 69-80 (2001)

Kenji Yamashiro 等：“组胺 H1 受体拮抗剂苯地拉明对内毒素诱导的葡萄膜炎期间白细胞浸润的抑制作用”实验眼科研究 73・1（2001）。