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Astaxanthin Pretreatment Attenuates Hepatic Ischemia Reperfusion-Induced Apoptosis and Autophagy via the ROS/MAPK Pathway in Mice.

AbstractBACKGROUND:
Hepatic ischemia reperfusion (IR) is an important issue in complex liver resection and liver transplantation. The aim of the present study was to determine the protective effect of astaxanthin (ASX), an antioxidant, on hepatic IR injury via the reactive oxygen species/mitogen-activated protein kinase (ROS/MAPK) pathway.
METHODS:
Mice were randomized into a sham, IR, ASX or IR + ASX group. The mice received ASX at different doses (30 mg/kg or 60 mg/kg) for 14 days. Serum and tissue samples at 2 h, 8 h and 24 h after abdominal surgery were collected to assess alanine aminotransferase (ALT), aspartate aminotransferase (AST), inflammation factors, ROS, and key proteins in the MAPK family.
RESULTS:
ASX reduced the release of ROS and cytokines leading to inhibition of apoptosis and autophagy via down-regulation of the activated phosphorylation of related proteins in the MAPK family, such as P38 MAPK, JNK and ERK in this model of hepatic IR injury.
CONCLUSION:
Apoptosis and autophagy caused by hepatic IR injury were inhibited by ASX following a reduction in the release of ROS and inflammatory cytokines, and the relationship between the two may be associated with the inactivation of the MAPK family.
AuthorsJingjing Li, Fan Wang, Yujing Xia, Weiqi Dai, Kan Chen, Sainan Li, Tong Liu, Yuanyuan Zheng, Jianrong Wang, Wenxia Lu, Yuqing Zhou, Qin Yin, Jie Lu, Yingqun Zhou, Chuanyong Guo
JournalMarine drugs (Mar Drugs) Vol. 13 Issue 6 Pg. 3368-87 (May 27 2015) ISSN: 1660-3397 [Electronic] Switzerland
PMID26023842 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Antioxidants
  • Cytokines
  • Inflammation Mediators
  • Reactive Oxygen Species
  • Xanthophylls
  • astaxanthine
  • Mitogen-Activated Protein Kinases
Topics
  • Animals
  • Antioxidants (administration & dosage, pharmacology)
  • Apoptosis (drug effects)
  • Autophagy (drug effects)
  • Cytokines (metabolism)
  • Disease Models, Animal
  • Dose-Response Relationship, Drug
  • Down-Regulation (drug effects)
  • Inflammation Mediators (metabolism)
  • Liver Diseases (etiology, prevention & control)
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Mitogen-Activated Protein Kinases (metabolism)
  • Reactive Oxygen Species (metabolism)
  • Reperfusion Injury (drug therapy)
  • Time Factors
  • Xanthophylls (administration & dosage, pharmacology)

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