LIN28A attenuates high glucose-induced retinal pigmented epithelium injury through activating SIRT1-dependent autophagy

AIM: To evaluate the effects of LIN28A (human) on high glucose-induced retinal pigmented epithelium (RPE) cell injury and its possible mechanism. METHODS: Diabetic retinopathy model was generated following 48h exposure to 30 mmol/L glucose (HG) in ARPE-19 cells. Quantitative real-time polymerase chain reaction (qRT-PCR) Western blot tested expression corresponding genes proteins. Cell viability as well apoptosis determined through counting kit-8 (CCK-8) flow cytometry assays. Immunofluorescence assay adopted autophagy activity. Caspase 3 activity, oxidative stress markers, cytokines were appraised adopting their commercial kits, respectively. Finally, cells preincubated with EX527, a Sirtuin 1 (SIRT1) inhibitor, prior HG stimulation validate regulatory RESULTS: downregulated HG-challenged overexpression greatly inhibited HG-induced loss, apoptosis, damage inflammatory response. Meanwhile, repressed SIRT1 challenged elevated after overexpression. In addition, treatment EX527 activated partly abolished protective role against HG-elicited inflammation CONCLUSION: exerts RPE damage, inflammation, via regulating SIRT1/autophagy.