Abstract: Objective To investigate the effect of miR-193a-3p on apoptosis induced by high glucose in human retinal vascular endothelial cells (HRECs) and its molecular mechanism. Methods HRECs cells were cultured in vitro to establish a high glucose (30 mmol/L glucose concentration) cell model. HRECs were divided into control group, model group, anti-miR-NC group, anti-miR-193a-3p group, model+miR-NC group, model+miR-193a-3p group, and model +LY294002 group. RT-qPCR was used to detect the expression of miR-193a-3p; Western blot was used to detect the expression levels of cleaved-caspase-3 (c-caspase-3), B cell lymphoma/leukemia-2(Bcl-2), phosphorylated phosphoinositide 3 kinase (p-PI3K) and phosphorylated protein kinase B (p-AKT); flow cytometry was used to detect cell apoptosis. Results Compared with the control group, the expressions of miR-193a-3p and Bcl-2 in the model group was significantly decreased, whereas apoptosis rate, and the expres- sion of c-caspase-3, P-PI3K and P-Akt was significantly increased (P＜0.05). Low expression of miR-193a-3p promotes c-caspase-3, p-PI3K and p-AKT expression, inhibited Bcl-2 expression, and promoted cell apoptosis (P＜0.05). High expression of miR-193a-3p can significantly reduce the effect of high glucose treatment on the apoptosis, c-caspase-3 and Bcl-2 expression of HRECs (P＜0.05). Inhibition of PI3K/AKT signaling pathway reversed the effect of high glucose treatment the apoptosis, c-caspase-3 and Bcl-2 expression of HRECs (P＜0.05). Conclusions miR-193a-3p could inhibit high glucose-induced apoptosis of HRECs by regulating PI3K/AKT signaling pathway.

Key words: miR-193a-3p, PI3K/AKT signaling pathway, human retinal vascular endothelial cell, high glucose, apoptosis