Department of Ophthalmology, Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai China.
Bioengineered. 2022 May;13(5):11636-11645. doi: 10.1080/21655979.2022.2070586.
The purpose of this study was to explore the mechanism by which puerarin regulated the expression of hypoxia-inducible factor 1α (HIF-1α) and vascular endothelial growth factor (VEGF) in humans' retinal pigment epithelial (RPE) cells under hypoxia. RPE cells (ARPE-19 and D407 cells) and a rat model of oxygen-induced retinopathy were used in the current study. Western blotting and ELISA were performed to detect the level of JAK2, phosphorylated JAK2, STAT3, phosphorylated STAT3, HIF-1α, and VEGF in cells. In addition, the interaction between JAK2 and STAT3 was determined using with a co-immunoprecipitation assay. We found puerarin inhibited hypoxia-induced upregulation of VEGF at both the mRNA and protein level via decreasing HIF-1α expression in RPE cells. Moreover, puerarin attenuated the interaction between JAK2 and STAT3, and subsequently blocking p-STAT3 nucleus translocation and . In conclusion, puerarin could effectively inhibit hypoxia-induced VEGF upregulation in RPE cells via mediated JAK2/STAT3 pathway.
本研究旨在探讨葛根素在缺氧条件下调节人视网膜色素上皮（RPE）细胞中缺氧诱导因子 1α（HIF-1α）和血管内皮生长因子（VEGF）表达的机制。本研究使用了 RPE 细胞（ARPE-19 和 D407 细胞）和氧诱导视网膜病变大鼠模型。采用 Western blot 和 ELISA 检测细胞中 JAK2、磷酸化 JAK2、STAT3、磷酸化 STAT3、HIF-1α 和 VEGF 的水平。此外，还通过共免疫沉淀测定 JAK2 和 STAT3 之间的相互作用。我们发现葛根素通过降低 RPE 细胞中 HIF-1α 的表达，抑制缺氧诱导的 VEGF 在 mRNA 和蛋白水平上的上调。此外，葛根素减弱了 JAK2 和 STAT3 之间的相互作用，进而阻止了 p-STAT3 核转位。综上所述，葛根素可以通过介导 JAK2/STAT3 通路有效抑制缺氧诱导的 RPE 细胞中 VEGF 的上调。
