Captopril alleviates oxidative damage in diabetic retinopathy

Aims: To primarily explore the mechanism of captopril in oxidative stress and investigate the link between captopril alleviated oxidative damage and diabetic retinopathy (DR). Main methods: Human retinal microvascular endothelial cells (HRMECs) were used for in vitro experiments and cultured in a 5.5 mM or 30 mM glucose medium. Sprague-Dawley rats were used for in vivo experiments, and parts of the rats were established for diabetic groups by injected streptozotocin (n = 10, each group). Both experiments had a captopril-treated group. The levels of total cholesterol (TC), reactive oxygen species (ROS), nitric oxide (NO), and human 3-nitrotyrosine (3-NT) were detected in assay kits and ELISA. Western blotting was used to detect the expression of steroid regulatory element binding protein 2 (SREBP2), inducible nitric oxide synthase (iNOS), vascular endothelial growth factor (VEGF), and endothelial nitric oxide synthase (eNOS). Hematoxylin-eosin staining and Evans blue were used to describe retinal histopathology. Key findings: The levels of TC, ROS, NO, and 3-NT were increased in the higher glucose groups compared with the normal controls during in vivo and in vitro experiments. Western blotting showed a higher level of SREBP2, iNOS, and VEGF and a lower eNOS level in the higher glucose groups. These results were reversed by captopril. Captopril relieved diabetic retinal vascular leakage. Significance: Our study suggested that captopril alleviates oxidative damage in DR due to creating lower peroxynitrite by decreasing ROS and NO, which may provide a visible direction for DR research.

Automated summary

This study demonstrates that captopril alleviates oxidative damage in diabetic retinopathy by reducing reactive oxygen species (ROS) and nitric oxide (NO) levels, thereby reducing peroxynitrite formation. These findings provide new directions for research in diabetic retinopathy.