Inhibition of galectin-3 ameliorates high-glucose-induced oxidative stress and inflammation in ARPE-19 cells.

Retinal pigment epithelium (RPE) has been found to be participated in the pathogenesis of DR in recent years. Galectin-3 (Gal-3) is involved in many diabetic complications and ophthalmological diseases. However, the role of Gal-3 in RPE cells in DR remains unknown. This study aims to investigate the role of Gal-3 in ARPE-19 cells under high glucose treatment. ARPE-19 cells were cultured under normal or high glucose (HG) for 48 h. Expression of Gal-3 was inhibited by Si-Gal-3 transfection. Apoptosis was checked by flow cytometry. Oxidative stress was checked by measuring ROS, MDA levels, and SOD activities. Occludin and ZO-1 expression were checked by immunofluorescence staining. Genes involved in inflammatory response were measured by real-time PCR and Western blot. Gal-3 expression could be increased by HG treatment in ARPE-19 cells. Gal-3 knockdown might reduce oxidative stress, apoptosis, and gene expression of VCAM-1, ICAM-1, and integrin-β1 induced by HG treatment. The gene expression of IL-1β could be markedly promoted by HG treatment and this increasement was partly alleviated by Gal-3 knockdown only at the mRNA level. The reduced expression of ZO-1 and occludin caused by HG could also be improved by Gal-3 knockdown. Gal-3 participated in increased oxidative stress and inflammatory response caused by HG in ARPE-19 cells.