目的:探讨内脏脂肪素(visfatin)、人血清淀粉样蛋白A(SAA)和肿瘤坏死因子（TNF-α）在2型糖尿病视网膜病变(DR)发病机制中的相关性。 方法：选择2型糖尿病患者无视网膜病变组35例，背景期DR组33例，增殖期DR组36例，同时选择40例健康正常人做对照组。应用酶联免疫分析法（ELISA）对DR患者血液中visfatin，SAA和TNF-α进行检测。 结果：2型DR患者的visfatin，SAA和TNF-α表达显著上调（P<0.01），较正常对照组有显著统计学差异（P<0-01），且与病情的进程呈正相关。视网膜受损程度与visfatin，SAA，空腹血糖（FPG）、糖化血红蛋白(HbA1c)呈正相关，与胰岛素的浓度成负相关。 结论：DR患者血浆visfatin水平升高，能反映患者眼底血管内皮功能紊乱情况和微动脉硬化严重程度，提示血浆visfatin水平可能与眼底动脉硬化的发生和发展密切相关；而SAA能刺激内皮细胞及单核细胞中组织因子的表达，促进血栓形成及斑块的不稳定；visfatin和SAA都能促进TNF-α分泌并在介导炎症反应中起到媒介作用，三者的异常表达具有促进眼内动脉重塑和新生内膜的生长作用，促进了2型DR患者病变的进展。

AIM: To investigate the relationship between visfatin, human serum amyloid A (SAA) and tumor necrosis factor α (TNF-α) and pathogenesis of type 2 diabetic retinopathy (DR). METHODS: Patients with type 2 diabetes mellitus (DM) without DR group comprised 35 individuals. Type 2 DM with nonproliferative DR group included 33 patients and type 2 DM with proliferative DR group was composed of 36 patients. The control group consisted of 40 healthy persons. ELISA was used to detect the contents of visfatin, SAA and TNF-α. RESULTS: The expressions of visfatin, SAA and TNF-α of patients from the 3 patients groups were significantly higher than those from the control group (P<0.01) and a significant difference existed between the patients groups and the control group (P<0.01). There was a positive correlation between these factors and the severity of disease. And the 3 factors were also positively correlated with fasting plasma glucose (FPG) and glycosylated hemoglobin (HbA1c) while negatively correlated with insulin concentration. CONCLUSION: Visfatin level of serum from patients with type 2 DR could reflect the fundus vascular endothelial dysfunction and the disease course of arteriosclerosis, which suggests that content of serum visfatin may be closely related with the occurrence and development of ocular fundus arteriosclerosis. And SAA could activate the expression of tissue factor in endothelial cells and monocytes, therefore, the formation of thrombosis and the instability of plaque was accelerated. visfatin and SAA could promote secretion of TNF-α and play the roles of medium in inducing inflammatory reaction. The abnormal expression of the three factors could accelerate the remodeling of internal ophthalmic artery and the growth effect of new intima and promote the disease evolution of type 2 DR.