Autophagy attenuates high glucose-induced oxidative injury to lens epithelial cells
Autophagy attenuates high glucose-induced oxidative injury to lens epithelial cells
复制标题
自噬减轻高糖诱导的晶状体上皮细胞氧化损伤
DOI：
10.1042/bsr20193006
复制
发表时间：
2020-03-31
影响因子：
4
通讯作者：
Huang, Yusen
中科院分区：
文献类型：
--
作者：
Liu, Xiaomin;Zhao, Xiaowen;Huang, Yusen
Purpose: Autophagic dysfunction and abnormal oxidative stress are associated with cataract. The purpose of the present study was to investigate the changes of cellular autophagy and oxidative stress and their association in lens epithelial cells (LECs) upon exposure to high glucose.Methods: Autophagy and oxidative stress-related changes were detected in streptozotocin-induced Type 1 diabetic mice and normal mouse LECs incubated in high glucose conditions. Rapamycin at a concentration of 100 nm/I or 50 mu M chloroquine was combined for analysis of the relationship between autophagy and oxidative stress. The morphology of LECs during autophagy was observed by transmission electron microscopy. The expressions of autophagy markers (LC3B and p62) were identified, as well as the key factors of oxidative stress (SOD2 and CAT) and mitochondriai reactive oxygen species (ROS) generation.Results: Transmission electron microscopy indicated an altered autophagy activity in diabetic mouse lens tissues with larger autophagosomes and multiple mitochondria. Regarding the expressions, LC3B was elevated, p62 was decreased first and then increased, and SOD2 and CAT were increased before a decrease during 4 months of follow-up in diabetic mice and 72 h of culture under high glucose for mouse LECs. Furthermore, rapamycin promoted the expressions of autophagy markers but alleviated those of oxidative stress markers, whereas chloroquine antagonized autophagy but enhanced oxidative stress by elevating ROS generation in LECs exposed to high glucose.Conclusions: The changes in autophagy and oxidative stress were fluctuating in the mouse LECs under constant high glucose conditions. Autophagy might attenuate high glucose-induced oxidative injury to LECs.
