Puerarin Protects Against Human Retinal Endothelial Cells Injury Induced By High Glucose Via Regulating Mir-16-5p/Casp1 Axis

We aimed to investigate the effects of puerarin on high glucose (HG)-induced human retinal endothelial cells (HRECs) injury. Cells were exposed to puerarin in the presence or absence of HG challenge. Cell viability was determined using a CCK-8 assay. Then, the levels of the oxidative stress-related factors were evaluated using corresponding kits. Pyroptosis was assessed by measurement of gasdermin-N domain (GSDMD-N) and caspase-1 (CASP I) expression. Subsequently, miR-16-5p expression was detected using RT-qPCR. The levels of oxidative stress and pyroptosis were examined after miR-16-5p silencing. The Starbase database predicted that CASP1 is a potential target of miR- I6-5p, which was verified through a luciferase reporter assay. Moreover, CASP1 expression was determined after miR-16-5p silencing in HG- stimulated HRECs with puerarin exposure. Results revealed that puerarin significantly enhanced cell viability and inhibited oxidative stress. Furthermore, puerarin markedly downregulated GSDMD-N and CASP1 expression, and miR-16-5p level was notably inhibited in HG-stimulated HRECs, which was reversed after puerarin intervention. Following transfection with miR-16-5p inhibitor, the effects of puerarin on cell viability, oxidative stress and pyroptosis were attenuated in HG-induced HRECs. CASP I was confirmed as a direct target gene of miR-16-5p. Taken together, puerarin alleviates oxidative stress and pyroptosis in HG-stimulated HRECs through regulating the miR-16-5p/CASP1 axis.