Diabetic retinopathy (DR) is a neurovascular complication of diabetes mellitus that leads to blindness in the working-age population. Retinal Müller cells proliferate and produce pro-angiogenic factors, including vascular endothelial growth factor (VEGF) and hepatocyte growth factor (HGF), via the reactive oxygen species (ROS)/thioredoxin interacting protein (TXNIP)/NACHT, LRR and PYD domain-containing protein 3 (NLRP3) inflammasome axis to promote proliferative DR. Epigallocatechin-3-gallate (EGCG) plays anti-oxidant, anti-inflammatory, anti-proliferative and anti-angiogenic roles in Müller cells. A prodrug of EGCG (pro-EGCG) enhances the bioavailability of EGCG. In an in vitro model of high glucose-stimulated Müller cells, pro-EGCG inhibited proliferation and pro-angiogenic factor production by down-regulating the activity of the ROS/TXNIP/NLRP3 inflammasome axis. In a mouse DR model, pro-EGCG reduced ROS accumulation, NLRP3 inflammasome activation, Müller cell proliferation, and production of the pro-angiogenic factors VEGF and HGF. In summary, pro-EGCG mitigated hyperglycaemia-challenged Müller cell proliferation and pro-angiogenic factor production by inhibiting ROS/TXNIP/NLRP3 inflammasome signalling, implying a potential therapeutic strategy for DR.

中文翻译：

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表没食子儿茶素-3-没食子酸酯的前药通过抑制视网膜Müller细胞中的ROS / TXNIP / NLRP3炎性体轴来减轻高葡萄糖诱导的促血管生成因子的产生。

糖尿病性视网膜病（DR）是糖尿病的神经血管并发症，导致劳动年龄人群失明。视网膜Müller细胞通过活性氧（ROS）/硫氧还蛋白相互作用蛋白（TXNIP）/ NACHT，LRR和PYD结构域增殖并产生促血管生成因子，包括血管内皮生长因子（VEGF）和肝细胞生长因子（HGF）。含有3号蛋白（NLRP3）的炎性轴，以促进增殖性DR。Epigallocatechin-3-gallate（EGCG）在Müller细胞中起抗氧化，抗炎，抗增殖和抗血管生成的作用。EGCG的前药（pro-EGCG）可提高EGCG的生物利用度。在高葡萄糖刺激的Müller细胞体外模型中，前EGCG通过下调ROS / TXNIP / NLRP3炎性体轴的活性来抑制增殖和促血管生成因子的产生。在小鼠DR模型中，促EGCG可降低ROS积累，NLRP3炎性体激活，Müller细胞增殖以及促血管生成因子VEGF和HGF的产生。总之，前EGCG通过抑制ROS / TXNIP / NLRP3炎症小体信号传导，减轻了高血糖症挑战的Müller细胞增殖和促血管生成因子的产生，这暗示了DR的潜在治疗策略。