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.
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Authors | Shuna Yu, Jie Zheng, Zhengchen Jiang, Caixing Shi, Jin Li, Xiaodong Du, Hailiang Wang, Jiying Jiang, Xin Wang |
Journal | International journal of molecular sciences
(Int J Mol Sci)
Vol. 14
Issue 9
Pg. 17680-93
(Aug 29 2013)
ISSN: 1422-0067 [Electronic] Switzerland |
PMID | 23994834
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Serotonin
- Malondialdehyde
- Superoxide Dismutase
- Aspartate Aminotransferases
- Caspase 3
- N-acetylserotonin
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Topics |
- Animals
- Apoptosis
(drug effects)
- Aspartate Aminotransferases
(blood)
- Blotting, Western
- Caspase 3
(metabolism)
- Immunohistochemistry
- In Situ Nick-End Labeling
- Liver
(drug effects, injuries, metabolism)
- Male
- Malondialdehyde
(blood)
- Mice
- Reperfusion Injury
(drug therapy, metabolism)
- Serotonin
(analogs & derivatives, therapeutic use)
- Superoxide Dismutase
(blood)
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