KIOM-79 prevents xylose-induced lens opacity and inhibits TGF-beta2 in human lens epithelial cells cultured under high glucose

Aim of the studyTo investigate the effects of KIOM-79 in preventing the development of diabetic complications, such as cataracts.Materials and methodsThe inhibitory effects of KIOM-79 were assessed in a model of xylose-induced lens opacity and on changes mediated by high levels of glucose in human lens epithelial (HLE-B3) cells.ResultsIn lenses treated with KIOM-79, opacity was significantly improved and glutathione (GSH) was increased compared to controls. In HLE-B3 cells treated with KIOM-79, high glucose-mediated increases in TGF-β2, αB-crystallin, and fibronectin were significantly inhibited in a dose-dependent manner. KIOM-79 decreased the phosphorylation of p-Smad2/3, pp38MAPK, pp44/42, and NF-κB signaling in cells grown under high glucose conditions.ConclusionKIOM-79 is protective against lens opacity and protects HLE-B3 cells from the toxic effects of high glucose. Therefore, KIOM-79 may provide a potential therapeutic approach for preventing diabetic complications, such as cataracts.

Graphical abstractKIOM-79 was protective against xylose-induced lens opacity and was increased glutathione levels in the lens. In the human lens epithelial (HLE-B3) cells treated with KIOM-79, the high glucose-mediated increase in αB-crystallin, fibronectin, and TGF-β2 was significantly inhibited in a dose-dependent manner. KIOM-79 may provide a potential therapeutic approach for preventing diabetic complications such as cataracts.Figure optionsDownload full-size imageDownload as PowerPoint slide