糖尿病性视网膜病变（DR）是世界性致盲的主要原因之一，视网膜水肿是DR视功能受损的一个重要原因及临床表现。血视网膜内屏障（iBRB）功能障碍及视网膜Müller细胞水通道蛋白4（AQP4）与内向整流性钾通道4.1（Kir4.l）之间的失藕联是糖尿病视网膜水肿形成的重要病理机制；目前中医药对糖尿病视网膜水肿作用机制的研究靶点多局限于视网膜血管内皮细胞，未见从Müller细胞AQP4与Kir4.l以及iBRB保护机制角度研究中医药对糖尿病视网膜水肿有何干预作用的报道。我们前期临床和实验研究均显示补肾活血法是治疗DR的一种有效治法。故本课题拟将体内与体外研究相结合，从iBRB损伤机制与保护机制、Müller细胞AQP4与Kir4.l之间失藕联等多个角度研究补肾活血法对早期糖尿病视网膜水肿形成有何干预作用及相关途径，以期从多层次揭示补肾活血法防治DR新的药物干预途径和可能的干预环节。

Diabetic retinopathy(DR) is one of the main cause of blindness worldwide. Retinal edema is an important pathological factor for visual disfunction and it is also ordinary clinical manifestation in DR. The significant pathological mechansim of diabetic retinal edema formation is the disfunction of inner blood-retinal barrier(iBRB), the interrupted couple between aquaporin-4 (AQP4) and inwardly rectifying potassium channel-4.1 (Kir4.1) in Müller cells. Up to now, the study reports about traditional Chinese medicine research targets for diabetic retinal edema are always confined to rather retinal vascular endothelial cells than AQP4 and Kir4.1 in Müller cells, or the protection mechanism of iBRB. Our previous clinical and experimental studies have shown BuShenHuoXueFa（补肾活血法）is an effective therapy of DR. Thus, combining in vivo and in vitro studies, basing on the iBRB damaged and protective mechanism as well as the imbalance of AQP4 and Kir4.1 expression in Müller cells, we hope to find the intervention effect and it's relative pathway on early diabetic retinal edema with BuShenHuoXueFa, and from multi-levels to elucidate the new intervention approaches and new possible links of BuShenHuoXueFa to prevent and cure DR.