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Astaxanthin Pretreatment Attenuates Hepatic Ischemia Reperfusion-Induced Apoptosis and Autophagy via the ROS/MAPK Pathway in Mice
Authors:Jingjing 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
Institution:1.Department of Gastroenterology, Shanghai Tenth People’s Hospital, Tongji University School of Medicine, Shanghai 200072, China; E-Mails: (J.L.); (F.W.); (Y.X.); (W.D.); (K.C.); (S.L.); (T.L.); (Y.Z.); (J.L.);2.The First Clinical Medical College of Nanjing Medical University, Nanjing 210029, China; E-Mails: (J.W.); (W.L.);3.The First Affiliated Hospital of Soochow University, Suzhou 215006, China; E-Mails: (Y.Z.); (Q.Y.)
Abstract:Background: 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.
Keywords:hepatic ischemia reperfusion  oxidative stress  astaxanthin  reactive oxygen species
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