糖尿病视网膜病变（DR）为糖尿病最主要的并发症和最常见的致盲性眼病，对该病的治疗一直是眼科的难点。血管内皮生长因子（VEGF）是DR发生发展以及致盲的关键因子，研究证实抗VEGF治疗可有效遏制DR的危害。由于中医药有着独特的优势，故临床开发抗VEGF中药有着现实意义。以往研究发现活血化瘀中药治疗DR可减少眼内VEGF的分泌，提示血瘀证和VEGF异常升高有相关性，但缺乏深入研究加以证实其相关性。我们研究发现ERK1/2信号通路参与调控DR疾病过程中视网膜及其特殊胶质细胞Muller细胞VEGF的分泌。在本项目中，我们拟利用糖尿病血瘀证大鼠血清刺激视网膜Muller细胞，建立病症结合的细胞模型，观察血瘀证对ERK1/2信号通路所介导的VEGF异常分泌的调控作用。通过研究结果揭示血瘀证与ERK1/2-VEGF通路在DR中的内在联系，为开发活血化瘀药物抗VEGF治疗DR奠定科学依据。

Diabetic retinopathy (DR) is one of the most common complications of diabetes. It brings serious harm impact on patient quality of life, and also becomes a heavy burden to society but treatment of it remains unsatisfactory. Vascular endothelial growth factor （VEGF）is a major pathogenic factor and a therapeutic target for diabetic retinopathy. However, the cellular mechanisms of VEGF remain virtually uninvestigated, making it difficult to design cellular target-based therapeutics for DR. On the other hand,the clinical application of these drugs remaining limitations which needed to be improved. Previous studies found that some Chinese traditional medicines especially the blood circulation drugs have the effect of reducing expression of VEGF in DR. These research suggesting that VEGF is closely associated with blood-stasis syndrome which need to deeply research. The project intends to use diabetic with blood-stasis syndrome rats' serum stimulating the retina Muller cell in vitro and observe the changes of VEGF releasing. The project also want to observe the regulation of VEGF secretion of ERK1/2 signaling pathways and nuclear transcription factor AP-1 changes. Hope that through these studies, to understand the effect of blood-stasis syndrome in DR on VEGF and the mechanism. At the same time, use different doses of Xuefuzhuyutang as blood circulation therapy to control groups to observe the therapeutic effect high VEGF releasing in DR. Results will illustrate a part of the pathological mechanism of stasis-blood syndrome in the DR and provide a scientific basis for the development of traditional Chinese medicine and the development of ophthalmic anti-VEGF treatment.