Abstract
The purpose of this study was to investigate the possible protective effect of N-acetylserotonin (NAS) against acute hepatic ischemia-reperfusion (I/R) injury in mice. Adult male mice were randomly divided into three groups: sham, I/R, and I/R + NAS. The hepatic I/R injury model was generated by clamping the hepatic artery, portal vein, and common bile duct with a microvascular bulldog clamp for 30 min, and then removing the clamp and allowing reperfusion for 6 h. Morphologic changes and hepatocyte apoptosis were evaluated by hematoxylin-eosin (HE) and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining, respectively. Activated caspase-3 expression was evaluated by immunohistochemistry and Western blot. The activation of aspartate aminotransferase (AST), malondialdehyde (MDA), and superoxide dismutase (SOD) was evaluated by enzyme-linked immunosorbent assay (ELISA). The data show that NAS rescued hepatocyte morphological damage and dysfunction, decreased the number of apoptotic hepatocytes, and reduced caspase-3 activation. Our work demonstrates that NAS ameliorates hepatic IR injury.
Highlights
Hepatic ischemia-reperfusion (I/R) injury, a major cause of liver damage during liver surgery and transplantation, triggers a series of molecular changes in hepatocytes, including insufficient ATP, increased production of reactive oxygen species (ROS), decline in ROS scavenging [1], and damage to mitochondria by accumulated free radicals, which perpetuates ROS generation
To determine whether NAS protects a variety of hepatocytes from I/R injury, we constructed a liver
Morphologic changes and apoptosis of hepatocytes were evaluated by hematoxylin-eosin (HE) and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining, respectively
Summary
Hepatic ischemia-reperfusion (I/R) injury, a major cause of liver damage during liver surgery and transplantation, triggers a series of molecular changes in hepatocytes, including insufficient ATP, increased production of reactive oxygen species (ROS), decline in ROS scavenging [1], and damage to mitochondria by accumulated free radicals, which perpetuates ROS generation. The overproduction of ROS leads to lipid peroxidation, mitochondrial membrane damage [2], release of cytochrome C (Cyt c) into the cytoplasm followed by caspase-3 activation, and the triggering of hepatocyte apoptosis [3,4]. Recent research has shown that NAS exhibits protective effects against peroxidative damage of neurons [18,19,20], lung epithelial cells [21], erythrocytes [22], testicular cells [23], retinal cells [24,25], and lymphocytes [26]
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