Astragaloside IV protects rat retinal capillary endothelial cells against high glucose-induced oxidative injury
Authors Qiao Y, Fan C, Tang M
Received 26 September 2017
Accepted for publication 22 November 2017
Published 13 December 2017 Volume 2017:11 Pages 3567—3577
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Dragan Hrncic
Peer reviewer comments 2
Editor who approved publication: Professor Manfred Ogris
Yuan Qiao, Chun-Lan Fan, Min-Ke Tang
School of Chinese Materia Medica, Beijing University of Chinese Medicine, Chaoyang District, Beijing, People’s Republic of China
Aim: Diabetic retinopathy is a microvascular complication of diabetes that leads to blindness. Hyperglycemia causes oxidative stress, which is an important cause in the pathogenesis of microangiopathy. The aim of this study was to investigate the potential protective effects of astragaloside IV (AS-IV) in retinal capillary endothelial cells (RCECs) incubated with high glucose conditions.
Methods and results: Based on rat RCECs cultured with high glucose (30 mM) in vitro, a significant increase in cell viability in rat RCECs incubated with both AS-IV and high glucose for 48 or 72 h by MTT assay. The increased viability was accompanied by decreased glucose transporter-1 expression using immunofluorescent assay. Meanwhile, AS-IV reduced intracellular hydrogen peroxide and superoxide, decreased mitochondrial reactive oxygen species in rat RCECs with high glucose by the fluorescent probes, and lowered malondialdehyde levels. In addition, AS-IV increased the activities of total superoxide dismutase, MnSOD, catalase, and glutathione peroxidase. The glutathione content also increased after AS-IV treatment. Furthermore, AS-IV reduced NADPH oxidase 4 expression by western blot method.
Conclusion: These results suggest that the main mechanism underlying the protective effects of AS-IV in high glucose-injured RCECs may be related to its antioxidative function.
Keywords: astragaloside IV, retinal capillary endothelial cells, oxidative stress, Glut1, Nox4
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