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Published on: January 12, 2024
Captopril alleviates oxidative damage in diabetic retinopathy
Xiang Gao1, Kou Liu1, Chengyang Hu2
1Department of Ophthalmology, The Second Affiliated Hospital of Anhui Medical University, Hefei, Anhui, China.
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.
Insights
Captopril treatment reduced oxidative damage and vascular leakage in diabetic retinopathy (DR) by decreasing reactive oxygen species (ROS) and nitric oxide (NO). This suggests captopril may be a potential therapeutic agent for DR.
Area of Science:
- Biomedical Science
- Ophthalmology
- Pharmacology
Background:
- Diabetic retinopathy (DR) is a microvascular complication of diabetes, characterized by oxidative stress.
- Oxidative damage plays a critical role in the pathogenesis of DR, leading to endothelial dysfunction and vascular leakage.
Purpose of the Study:
- To investigate the protective mechanisms of captopril against oxidative stress in DR.
- To explore the relationship between captopril-mediated reduction of oxidative damage and its therapeutic effects on DR.
Main Methods:
- In vitro studies utilized human retinal microvascular endothelial cells (HRMECs) cultured in high glucose conditions.
- In vivo studies involved Sprague-Dawley rats induced with diabetes using streptozotocin.
- Biochemical assays measured total cholesterol, reactive oxygen species (ROS), nitric oxide (NO), and 3-nitrotyrosine (3-NT).
- Western blotting assessed protein expression of SREBP2, iNOS, VEGF, and eNOS.
- Histopathological analysis included Hematoxylin-eosin staining and Evans blue assay.
Main Results:
- High glucose levels significantly increased TC, ROS, NO, and 3-NT levels in both in vitro and in vivo models.
- Elevated SREBP2, iNOS, and VEGF, along with decreased eNOS expression, were observed under high glucose conditions.
- Captopril treatment reversed these detrimental changes, reducing oxidative stress markers.
- Captopril effectively alleviated diabetic retinal vascular leakage.
Conclusions:
- Captopril mitigates oxidative damage in DR by reducing ROS and NO levels, thereby decreasing peroxynitrite formation.
- These findings highlight captopril's potential as a therapeutic strategy for managing diabetic retinopathy.
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