AbstractDiabetic retinopathy (DR) is a significant complication of diabetes that often leads to blindness, impacting Müller cells, the primary retinal macroglia involved in DR pathogenesis. Reactive oxygen species (ROS) play a crucial role in the development of DR. The objective of this study was to investigate the involvement of sestrin2 in DR using a high‐glucose (HG)‐induced Müller cell model and assessing cell proliferation with 5‐ethynyl‐2‐deoxyuridine (EdU) labeling. Following this, sestrin2 was upregulated in Müller cells to investigate its effects on ROS, tube formation, and inflammation both in vitro and in vivo, as well as its interaction with the nuclear factor erythroid2‐related factor 2 (Nrf2) signaling pathway. The findings demonstrated a gradual increase in the number of EdU‐positive cells over time, with a subsequent decrease after 72 h of exposure to high glucose levels. Additionally, the expression of sestrin2 exhibited a progressive increase over time, followed by a decrease at 72 h. The rh‐sestrin2 treatment suppressed the injury of Müller cells, decreased ROS level, and inhibited the tube formation. Rh‐sestrin2 treatment enhanced the expression of sestrin2, Nrf
📖 افتح في inklap 🔗 DOI 📮 اطلب بحثاً