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Protective effect of N-acetylserotonin against acute hepatic ischemia-reperfusion injury in mice.

Yu S, Zheng J, Jiang Z, Shi C, Li J, Du X, Wang H, Jiang J, Wang X - Int J Mol Sci (2013)

Bottom Line: Morphologic changes and hepatocyte apoptosis were evaluated by hematoxylin-eosin (HE) and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining, respectively.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.

View Article: PubMed Central - PubMed

Affiliation: Departments of Anatomy, Weifang Medical University, Weifang 261053, China.

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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Related in: MedlinePlus

Effects of I/R and NAS treatment on SOD levels. (a): sham, mice were subjected to all surgical procedures except for liver I/R; (b): I/R, the mice underwent the liver I/R operation; (c): I/R + NAS, NAS (5 mg/kg) was administered by i.p. injection 30 min before ischemia. Note the significant decrease in SOD in the I/R group compared with the sham group (p < 0.01) and the increase in the I/R + NAS group compared with the I/R group (p < 0.01). Error bars represent SD (n = 6). The annotation ** indicates a p value < 0.01 vs. sham group. The annotation # indicates a p value < 0.05 vs. I/R group.
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f5-ijms-14-17680: Effects of I/R and NAS treatment on SOD levels. (a): sham, mice were subjected to all surgical procedures except for liver I/R; (b): I/R, the mice underwent the liver I/R operation; (c): I/R + NAS, NAS (5 mg/kg) was administered by i.p. injection 30 min before ischemia. Note the significant decrease in SOD in the I/R group compared with the sham group (p < 0.01) and the increase in the I/R + NAS group compared with the I/R group (p < 0.01). Error bars represent SD (n = 6). The annotation ** indicates a p value < 0.01 vs. sham group. The annotation # indicates a p value < 0.05 vs. I/R group.

Mentions: To determine whether NAS protects hepatocytes against oxidative stress damage, SOD and MDA concentrations in the liver homogenates of the sham and experimental groups were measured. SOD activities of the sham, I/R, and I/R + NAS groups were 104.6 ± 12.4, 68.6 ± 15.9 and 91.6 ± 13.9 U/mg protein, respectively. MDA contents were 1.1 ± 0.2, 2.4 ± 0.5 and 1.4 ± 0.2 nmol/mg protein, respectively. NAS administration caused a significant decrease in MDA content and increased SOD enzyme activity compared with the I/R group (p < 0.01) (Figures 4 and 5).


Protective effect of N-acetylserotonin against acute hepatic ischemia-reperfusion injury in mice.

Yu S, Zheng J, Jiang Z, Shi C, Li J, Du X, Wang H, Jiang J, Wang X - Int J Mol Sci (2013)

Effects of I/R and NAS treatment on SOD levels. (a): sham, mice were subjected to all surgical procedures except for liver I/R; (b): I/R, the mice underwent the liver I/R operation; (c): I/R + NAS, NAS (5 mg/kg) was administered by i.p. injection 30 min before ischemia. Note the significant decrease in SOD in the I/R group compared with the sham group (p < 0.01) and the increase in the I/R + NAS group compared with the I/R group (p < 0.01). Error bars represent SD (n = 6). The annotation ** indicates a p value < 0.01 vs. sham group. The annotation # indicates a p value < 0.05 vs. I/R group.
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC3794748&req=5

f5-ijms-14-17680: Effects of I/R and NAS treatment on SOD levels. (a): sham, mice were subjected to all surgical procedures except for liver I/R; (b): I/R, the mice underwent the liver I/R operation; (c): I/R + NAS, NAS (5 mg/kg) was administered by i.p. injection 30 min before ischemia. Note the significant decrease in SOD in the I/R group compared with the sham group (p < 0.01) and the increase in the I/R + NAS group compared with the I/R group (p < 0.01). Error bars represent SD (n = 6). The annotation ** indicates a p value < 0.01 vs. sham group. The annotation # indicates a p value < 0.05 vs. I/R group.
Mentions: To determine whether NAS protects hepatocytes against oxidative stress damage, SOD and MDA concentrations in the liver homogenates of the sham and experimental groups were measured. SOD activities of the sham, I/R, and I/R + NAS groups were 104.6 ± 12.4, 68.6 ± 15.9 and 91.6 ± 13.9 U/mg protein, respectively. MDA contents were 1.1 ± 0.2, 2.4 ± 0.5 and 1.4 ± 0.2 nmol/mg protein, respectively. NAS administration caused a significant decrease in MDA content and increased SOD enzyme activity compared with the I/R group (p < 0.01) (Figures 4 and 5).

Bottom Line: Morphologic changes and hepatocyte apoptosis were evaluated by hematoxylin-eosin (HE) and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining, respectively.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.

View Article: PubMed Central - PubMed

Affiliation: Departments of Anatomy, Weifang Medical University, Weifang 261053, China.

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.

Show MeSH
Related in: MedlinePlus