Puerarin suppresses hypoxia-induced vascular endothelial growth factor upregulation in human retinal pigmented epithelial cells by blocking JAK2/STAT3 pathway

The purpose of this study was to explore the mechanism by which puerarin regulated the expression of hypoxia-inducible factor 1 alpha (HIF-1 alpha) 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-1 alpha, 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-1 alpha expression in RPE cells. Moreover, puerarin attenuated the interaction between JAK2 and STAT3, and subsequently blocking p-STAT3 nucleus translocation in vitro and in vivo. In conclusion, puerarin could effectively inhibit hypoxia-induced VEGF upregulation in RPE cells via mediated JAK2/STAT3 pathway.

Automated summary

This study found that puerarin inhibited the upregulation of VEGF in RPE cells under hypoxia by decreasing the expression of HIF-1α. Additionally, puerarin attenuated the interaction between JAK2 and STAT3, leading to the prevention of p-STAT3 nucleus translocation. These findings suggest that puerarin effectively inhibits hypoxia-induced VEGF upregulation in RPE cells through the JAK2/STAT3 pathway.