Astaxanthin inhibits expression of retinal oxidative stress and inflammatory mediators in streptozotocin-induced diabetic rats
Journal
PLoS ONE
Journal Volume
11
Journal Issue
1
Pages
e0146438
Date Issued
2016
Author(s)
Abstract
Purpose We evaluated whether orally administered astaxanthin (AST) protects against oxidative damage in the ocular tissues of streptozotocin (STZ)-induced diabetic rats. Methods and Results Fifty 6-week-old female Wistar rats were randomly assigned to receive an injection of STZ to induce diabetes (n = 40) or to remain uninduced (n = 10). The diabetic rats were randomly selected into four groups and they were separately administered normal saline, 0.6 mg/kg AST, 3 mg/kg AST, or 0.5 mg/kg lutein daily for eight weeks. Retinal functions of each group were evaluated by electroretinography. The expression of oxidative stress and inflammatory mediators in the ocular tissues was then assessed by immunohistochemistry, western blot analysis, ELISA, RT-PCR, and electrophoretic mobility shift assay (EMSA). Retinal functions were preserved by AST and lutein in different levels. Ocular tissues from ASTand lutein-treated rats had significantly reduced levels of oxidative stress mediators (8-hydroxy-2'-deoxyguanosine, nitrotyrosine, and acrolein) and inflammatory mediators (intercellular adhesion molecule-1, monocyte chemoattractant protein-1, and fractalkine), increased levels of antioxidant enzymes (heme oxygenase-1 and peroxiredoxin), and reduced activity of the transcription factor nuclear factor-kappaB (NF-?B). Conclusion The xanthophyll carotenoids AST and lutein have neuroprotective effects and reduce ocular oxidative stress, and inflammation in the STZ diabetic rat model, which may be mediated by downregulation of NF-?B activity. ? 2016 Yeh et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
SDGs
Other Subjects
3 nitrotyrosine; 8 hydroxydeoxyguanosine; acrolein; astaxanthin; fractalkine; heme oxygenase 1; immunoglobulin enhancer binding protein; intercellular adhesion molecule 1; monocyte chemotactic protein 1; peroxiredoxin; sodium chloride; streptozocin; xanthophyll; antioxidant; astaxanthin; autacoid; glucose blood level; immunoglobulin enhancer binding protein; intercellular adhesion molecule 1; messenger RNA; monocyte chemotactic protein 1; protective agent; xanthophyll; animal experiment; animal model; animal tissue; Article; controlled study; diabetic retinopathy; down regulation; drug megadose; electroretinography; enzyme activity; enzyme linked immunosorbent assay; female; gel mobility shift assay; immunohistochemistry; low drug dose; neuroprotection; nonhuman; oxidative stress; pathogenesis; protein expression; rat; real time polymerase chain reaction; Western blotting; animal; aqueous humor; body weight; Diabetes Mellitus, Experimental; drug effects; gene expression; gene expression regulation; genetics; glucose blood level; metabolism; oxidative stress; pathology; retina; retina ganglion cell; Animals; Antioxidants; Aqueous Humor; Blood Glucose; Body Weight; Chemokine CCL2; Diabetes Mellitus, Experimental; Electroretinography; Female; Gene Expression; Gene Expression Regulation, Enzymologic; Inflammation Mediators; Intercellular Adhesion Molecule-1; Lutein; NF-kappa B; Oxidative Stress; Protective Agents; Rats; Retina; Retinal Ganglion Cells; RNA, Messenger; Xanthophylls
Publisher
Public Library of Science
Type
journal article