Oral Astaxanthin Supplementation Prevents Peritoneal Fibrosis in Rats

Perit Dial Int. 2015 Sep-Oct;35(5):506-16. doi: 10.3747/pdi.2013.00317. Epub 2014 Oct 7.

Abstract

Background: Preventing peritoneal damage during peritoneal dialysis is critical. Reactive oxygen species (ROS) have an important role in peritoneal damage; however, few studies have investigated this. We aimed to determine the effects of oral astaxanthin (AST) supplementation in a peritoneal fibrosis (PF) rat model.

Methods: Thirty-seven Sprague-Dawley rats were divided into 5 groups: Control 1 (fed a normal diet without stimulation), Control 2 (fed an AST-supplemented diet without stimulation), Group 1 (fed a normal diet with 8% chlorhexidine gluconate [CG] stimulation for 3 weeks), Group 2 (fed a 0.06% AST-supplemented diet with CG stimulation), and Group 3 (fed a 0.06% AST-supplemented diet that was initiated 4 weeks before CG stimulation). Peritoneal fibrosis, vascular proliferation, and fibrosis-related factor expression were examined.

Results: Peritoneal thickness was significantly suppressed by AST supplementation. Astaxanthin diminished the number of CD68-, 8-hydroxy-2'-deoxyguanosine (8-OHdG)-, and monocyte chemoattractant protein-1 (MCP-1)-positive cells. Type 3 collagen, tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and MCP-1 mRNA expression was significantly lower in Group 3 than in Group 1. Increased transforming growth factor-β (TGF-β) and Snail mRNA expression, vascular density, and the number of α-smooth muscle actin (α-SMA)-positive cells were also decreased in Group 3.

Conclusion: Astaxanthin suppressed PF development through the inhibition of inflammation and oxidation in PF rats. It appears that the anti-oxidative agent AST may be useful for the prevention of peritoneal damage.

Keywords: Anti-inflammation; anti-oxidant; astax-anthin; peritoneal fibrosis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 8-Hydroxy-2'-Deoxyguanosine
  • Administration, Oral
  • Animals
  • Anti-Inflammatory Agents / therapeutic use*
  • Antioxidants / therapeutic use*
  • Chemokine CCL2 / genetics
  • Chemokine CCL2 / metabolism
  • Collagen Type III / metabolism
  • Deoxyguanosine / analogs & derivatives
  • Deoxyguanosine / metabolism
  • Disease Models, Animal
  • Fluorescent Antibody Technique
  • Immunohistochemistry
  • Inflammation / drug therapy
  • Interleukin-1beta / metabolism
  • Male
  • Oxidative Stress / drug effects
  • Peritoneal Dialysis
  • Peritoneal Fibrosis / metabolism
  • Peritoneal Fibrosis / prevention & control*
  • Peritoneum / metabolism
  • Peritoneum / pathology*
  • Rats
  • Rats, Sprague-Dawley
  • Real-Time Polymerase Chain Reaction
  • Tumor Necrosis Factor-alpha / metabolism
  • Xanthophylls / therapeutic use

Substances

  • Anti-Inflammatory Agents
  • Antioxidants
  • Ccl2 protein, rat
  • Chemokine CCL2
  • Collagen Type III
  • Interleukin-1beta
  • Tumor Necrosis Factor-alpha
  • Xanthophylls
  • 8-Hydroxy-2'-Deoxyguanosine
  • astaxanthine
  • Deoxyguanosine