Abstract

Background Diabetic cataract is a common ocular complication of diabetes. Circular RNA (circRNA) can participate in a variety of regulatory processes of a variety of eye diseases, including diabetic cataract. Objective Nowadays, the biological mechanism underlying circ_0024037 during diabetic cataract is not completely understood. This study was designed to explore the biological role of circ_0024037 in high glucose (HG)-induced lens epithelial damage. Result Circ_0024037 and TP53INP1 were significantly up-regulated while miR-199a-5p was significantly down-regulated in the diabetic cataract tissues and HG-induced human lens epithelial cells (HLECs). Knockdown of circ_0024037 significantly promoted the HG-induced HLECs cell proliferation, inhibited apoptosis, decreased MDA level as well as increased GSH-PX level. The dual-luciferase reporter assay and RIP assay showed that circ_0024037 served as a sponge of miR-199a-5p and miR-199a-5p could directly target TP53INP1 in HLECs. Conclusion Circ_0024037 knockdown protected HLECs from the HG-induced dysfunction by regulating the miR-199a-5p/TP53INP1 pathway in diabetic cataract. Our findings provid novel insights into the pathogenesis of diabetic cataract. Highlights Circ_0024037 is up-regulated in diabetic cataract; Circ_0024037 regulates proliferation, apoptosis, MDA, and GSH-PX level in high- glucose-induced HLECs; Circ_0024037/miR-199a-5p/TP53INP1 involves in the progression of diabetic cataract.