Procyanidin protects human retinal pigment epithelial cells from high glucose by inhibiting autophagy

Purpose The damage of hyperglycemia to the retinal pigment epithelial (RPE) cells is a critical event in diabetic retinopathy (DR). Procyanidin (PC), a kind of polyphenol compounds, has shown to be effective in preventing and treating diabetes as well as its complications, in which autophagy disorder is involved in the pathological mechanism. However, it remains unclear whether PC can play a protective role in DR by regulating the autophagy of RPE. Here, the effect of PC on RPE under high glucose conditions and the role of autophagy were investigated. Materials and Methods The cell viability of ARPE-19, a human RPE cell line, was detected by cell counting kit-8 (CCK-8) and the apoptosis rate was measured by flow cytometry. The protein expressions of apoptosis markers, including Bax, Bcl-2, and Caspase-3, as well as autophagy markers including LC3, p62, p53, and mTOR were detected by Western blotting. Autophagic flux in ARPE-19 cells was detected by transfection with Ad-mCherry-GFP-LC3B. Results Under high glucose conditions, the viability of ARPE-19 was decreased and the apoptosis rate increased, the protein expressions of Bax, Caspase-3, LC3-II/LC3-I, and p-p53 were all increased and the expressions of Bcl-2, p62, and p-mTOR decreased, and autophagic flux was increased compared with that of the controls. Treatment with PC weakened all these changes caused by high glucose. When rapamycin (RPM), an autophagy agonist was added, the cell viability of ARPE-19 by PC treatment was decreased while the apoptosis was increased. Conclusions Our findings indicate that through the p53/mTOR autophagy pathway, PC may protect RPE cells from high glucose-induced injury.

Automated summary

High glucose damages RPE cells, but procyanidin (PC) may protect them through the p53/mTOR autophagy pathway. This study found that PC treatment under high glucose conditions weakened cell viability decrease, apoptosis increase, and autophagy marker expression changes in ARPE-19 cells.