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Astringinin-mediated attenuation of the hepatic injury following trauma-hemorrhage.

Abstract
Although astringinin administration under adverse circulatory conditions is known to be protective, the mechanism by which astringinin produces the salutary effects remains unknown. We hypothesize that astringinin administration in males following trauma-hemorrhage decreases cytokine production and protects against hepatic injury. Male Sprague-Dawley rats underwent trauma-hemorrhage (mean blood pressure: 40 mmHg for 90 min, then resuscitation). Different doses of astringinin (0.01, 0.03, 0.1, 0.3 mg/kg of body weight) or vehicle were administered intravenously during resuscitation. Concentrations of plasma aspartate aminotransferase (AST) with alanine aminotransferase (ALT) and various hepatic parameters were measured (n = 8 rats/group) at 24 h after resuscitation. One-way ANOVA and Tukey testing were used for statistical analysis. Trauma-hemorrhage significantly increased plasma AST and ALT levels at 24 h postresuscitation; there was a dose-related benefit when astringinin was administered at doses of 0.01 to 0.3 mg/kg. In astringinin-treated (0.3 mg/kg) rats subjected to trauma-hemorrhage, there were significant improvements in liver myeloperoxidase (MPO) activity (237.80 +/- 45.89 vs. 495.95 +/- 70.64 U/mg protein, P < 0.05), interleukin-6 (IL-6) levels (218.54 +/- 34.52 vs. 478.60 +/- 76.21 pg/mg protein, P < 0.05), cytokine-induced neutrophil chemoattractant (CINC)-1 (88.32 +/- 20.33 vs. 200.70 +/- 32.68 pg/mg protein, P < 0.05), CINC-3 (110.83 +/- 26.63 vs. 290.14 +/- 76.82 pg/mg protein, P < 0.05) and intercellular adhesion molecule (ICAM)-1 concentrations (1,868.5 +/- 211.5 vs. 3,645.0 +/- 709.2 pg/mg protein, P < 0.05), as well as in histology. Results show that astringinin significantly attenuates proinflammatory responses and hepatic injury after trauma-hemorrhage. In conclusion, the salutary effects of astringinin administration on attenuation of hepatic injury following trauma-hemorrhage are likely due to reduction of pro-inflammatory mediator levels.
AuthorsYi-Shun Huang, Fu-Chao Liu, Allen H Li, Ying-Tung Lau, Huang-Ping Yu
JournalThe Chinese journal of physiology (Chin J Physiol) Vol. 54 Issue 3 Pg. 183-9 (Jun 30 2011) ISSN: 0304-4920 [Print] India
PMID21789900 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Chemokine CXCL1
  • Cxcl1 protein, rat
  • Interleukin-6
  • Stilbenes
  • Intercellular Adhesion Molecule-1
  • 3,3',4,5'-tetrahydroxystilbene
  • Peroxidase
  • Aspartate Aminotransferases
  • Alanine Transaminase
Topics
  • Alanine Transaminase (blood)
  • Animals
  • Aspartate Aminotransferases (blood)
  • Chemokine CXCL1 (metabolism)
  • Dose-Response Relationship, Drug
  • Humans
  • Intercellular Adhesion Molecule-1 (metabolism)
  • Interleukin-6 (metabolism)
  • Liver (drug effects, enzymology, metabolism)
  • Liver Diseases (drug therapy, enzymology, immunology, metabolism)
  • Male
  • Peroxidase (metabolism)
  • Rats
  • Rats, Sprague-Dawley
  • Resuscitation (methods)
  • Shock, Hemorrhagic (enzymology, immunology, metabolism)
  • Stilbenes (pharmacology)

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