Astaxanthin Inhibits Expression of Retinal Oxidative Stress and Inflammatory Mediators in Streptozotocin-Induced Diabetic Rats

Po-Ting Yeh, Hsin-Wei Huang, Chung-May Yang, Wei-Shiung Yang, Chang-Hao Yang

Research output: Contribution to journalArticlepeer-review

103 Citations (Scopus)


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 AST- and 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-κB).

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-κB activity.

Original languageEnglish
Pages (from-to)e0146438
JournalPLoS ONE
Issue number1
Publication statusPublished - 2016
Externally publishedYes


  • Animals
  • Antioxidants/pharmacology
  • Aqueous Humor/metabolism
  • Blood Glucose
  • Body Weight
  • Chemokine CCL2/metabolism
  • Diabetes Mellitus, Experimental/drug therapy
  • Electroretinography
  • Female
  • Gene Expression
  • Gene Expression Regulation, Enzymologic/drug effects
  • Inflammation Mediators/metabolism
  • Intercellular Adhesion Molecule-1/metabolism
  • Lutein/pharmacology
  • NF-kappa B/genetics
  • Oxidative Stress/drug effects
  • Protective Agents
  • RNA, Messenger/genetics
  • Rats
  • Retina/drug effects
  • Retinal Ganglion Cells/drug effects
  • Xanthophylls/pharmacology


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