Abstract: Objective     To investigate the effect and molecular mechanism of Morroniside (Mor) on high glucose-induced human retinal microvascular endothelial cells (HRECs) oxidative stress and apoptosis. Methods    HRECs were divided into a control (Con) group, a high glucose (HG) group, a HG+Mor-low dose (L) group, a HG+Mor-medium dose (M) group, a HG+Mor-high dose (H) Group, a HG+anti-miR-NC group, a HG+anti-miR-483-5p group, a HG+Mor+miR-NC group, a HG+Mor+miR-483-5p group. The apoptosis rate and ROS level of HRECs were detected by using flow cytometry. MDA level and SOD activity were assessed by using enzyme-linked immunosorbent assay. miR-483-5p expression was detected by using Real-time quantitative PCR.    Results   Compared with the Con group, the apoptosis rate, ROS and MDA levels of HRECs in the HG group were significantly increased (P<0.05), SOD activity was significantly decreased (P<0.05), and miR-483-5p expression was significantly increased (P<0.05). Compared with the HG group, the apoptosis rate, ROS and MDA levels of HRECs in the HG+Mor-L group, HG+Mor-M group, and HG+Mor-H group were significantly reduced (P<0.05), and SOD activity was significantly increased (P<0.05), miR-483-5p expression was significantly reduced (P<0.05). Compared with the HG+anti-miR-NC group, the apoptosis rate, ROS and MDA levels of HRECs in the HG+anti-miR-483-5p group were significantly reduced (P<0.05), and SOD activity was significantly increased (P<0.05). Compared with the HG+Mor+miR-NC group, the apoptosis rate, ROS and MDA levels of HRECs in the HG+Mor+miR-483-5p group were significantly increased (P<0.05), and SOD activity was significantly decreased (P<0.05).    Conclusions    Morroniside inhibits high glucose-induced HRECs oxidative stress and apoptosis by down-regulating miR-483-5p expression.

Key words: Morroniside; ,  , miR-483-5p; ,  , High glucose; ,  , Retina; ,  , Vascular endothelial cells, Oxidative stress; ,  , Apoptosis