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目的 探讨粘附分子在糖尿病视网膜病变（ Ｄ Ｒ） 发病中的作用。方法 应用链脲佐菌素（ Ｓ Ｔ Ｚ） 建立糖尿病大鼠模型，分别于成模后３ 个月和６ 个月时经光镜和透射电镜观察视网膜的形态学改变。应用免疫组化方法及微机图像处理系统，对视网膜组织细胞间粘附分子１（ Ｉ Ｃ Ａ Ｍ１） 及整合素族 Ｃ Ｄ６１ 的分布与含量进行动态观察与分析；应用流式细胞术测定循环血中粒细胞表面β２ 整合素族 Ｃ Ｄ１１ａ 、 Ｃ Ｄ１１ｂ 的表达。结果 病变３ 月组已有 Ｉ Ｃ Ａ Ｍ１ 及 Ｃ Ｄ６１ 的表达明显增加，并随病程延长表达进一步增多，而在正常对照组未见明显表达（ Ｐ＜ ０ ．０１） 。糖尿病大鼠粒细胞表面抗原 Ｃ Ｄ１１ａ 、 Ｃ Ｄ１１ｂ 阳性细胞群体所占的比例较对照组显著升高（ Ｐ＜ ０ ．００１） 。视网膜毛细血管基底膜厚度与 Ｉ Ｃ Ａ Ｍ１ 、 Ｃ Ｄ６１ 表达灰度值呈显著正相关（ ｒ ＝ ０ ．７７２ ，０ ．６９４ ， Ｐ＜ ０ ．０５） 。结论 粘附分子与其配基过度表达，加重内皮细胞损伤及微血管栓塞，很可能是导致 Ｄ Ｒ 发生中进展性微血管病变的重要因素之一。
Objective To investigate the role of adhesion molecules in the pathogenesis of diabetic retinopathy (DR). Methods Diabetic rats were induced by streptozotocin (STZ) and the morphological changes of the retina were observed by light microscope and transmission electron microscope at 3 and 6 months after the model was established. Immunohistochemistry and computerized image processing system were used to observe and analyze the distribution and content of intracellular adhesion molecule1 (I C A M1) and integrin C D61 in retina. Flow cytometry The levels of β2 integrin C D11a and C D11b on the surface of granulocytes in circulating blood were measured. Results The expression of I C A M1 and C D61 in the 3-month-old group was significantly increased and further increased with the prolongation of the disease. However, it was not found in the normal control group (P <0.01). The percentage of granulocyte surface antigen C D11a and C D11b positive cells in diabetic rats was significantly higher than that in the control group (P <0.001). The retinal capillary basement membrane thickness and I C A M 1, C D61 expression gray value was significantly correlated (r = 0.772, 0.694, P <0.05). Conclusions The overexpression of adhesion molecules and their ligands may aggravate endothelial cell injury and microvascular embolism and may be one of the important factors leading to progressive microvascular disease in D R.