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10.3747/pdi.2013.00317

http://scihub22266oqcxt.onion/10.3747/pdi.2013.00317
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C4597983!4597983 !25292409
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suck abstract from ncbi


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pmid25292409
      Perit+Dial+Int 2015 ; 35 (5 ): 506-16
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  • Oral Astaxanthin Supplementation Prevents Peritoneal Fibrosis in Rats #MMPMID25292409
  • Wakabayashi K ; Hamada C ; Kanda R ; Nakano T ; Io H ; Horikoshi S ; Tomino Y
  • Perit Dial Int 2015[Sep]; 35 (5 ): 506-16 PMID25292409 show ga
  • 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-? (TNF-?), interleukin-1? (IL-1?), and MCP-1 mRNA expression was significantly lower in Group 3 than in Group 1. Increased transforming growth factor-? (TGF-?) and Snail mRNA expression, vascular density, and the number of ?-smooth muscle actin (?-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.
  • |8-Hydroxy-2'-Deoxyguanosine [MESH]
  • |Administration, Oral [MESH]
  • |Animals [MESH]
  • |Anti-Inflammatory Agents/*therapeutic use [MESH]
  • |Antioxidants/*therapeutic use [MESH]
  • |Chemokine CCL2/genetics/metabolism [MESH]
  • |Collagen Type III/metabolism [MESH]
  • |Deoxyguanosine/analogs & derivatives/metabolism [MESH]
  • |Disease Models, Animal [MESH]
  • |Fluorescent Antibody Technique [MESH]
  • |Immunohistochemistry [MESH]
  • |Inflammation/drug therapy [MESH]
  • |Interleukin-1beta/metabolism [MESH]
  • |Male [MESH]
  • |Oxidative Stress/drug effects [MESH]
  • |Peritoneal Dialysis [MESH]
  • |Peritoneal Fibrosis/metabolism/*prevention & control [MESH]
  • |Peritoneum/metabolism/*pathology [MESH]
  • |Rats [MESH]
  • |Rats, Sprague-Dawley [MESH]
  • |Real-Time Polymerase Chain Reaction [MESH]
  • |Tumor Necrosis Factor-alpha/metabolism [MESH]


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