TY - JOUR
T1 - Astringinin-mediated attenuation of the hepatic injury following trauma-hemorrhage
AU - Huang, Yi Shun
AU - Liu, Fu-Chao
AU - Li, Allen H.
AU - Lau, Ying-Tung
AU - Yu, Huang-Ping
PY - 2011
Y1 - 2011
N2 - 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 traumahemorrhage are likely due to reduction of pro-inflammatory mediator levels.
AB - 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 traumahemorrhage are likely due to reduction of pro-inflammatory mediator levels.
KW - Adhesion molecule
KW - Astringinin
KW - Chemokine
KW - Cytokine
KW - Hemorrhagic shock
UR - http://www.scopus.com/inward/record.url?scp=79954508264&partnerID=8YFLogxK
U2 - 10.4077/CJP.2011.AMM024
DO - 10.4077/CJP.2011.AMM024
M3 - 文章
C2 - 21789900
AN - SCOPUS:79954508264
SN - 0304-4920
VL - 54
SP - 5
JO - Chinese Journal of Physiology
JF - Chinese Journal of Physiology
IS - 3
ER -