Ghrelin contributes to protection of hepatocellular injury induced by ischaemia/reperfusion
Article first published online: 2 SEP 2013
© 2013 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
Volume 34, Issue 4, pages 567–575, April 2014
How to Cite
Liver Int. 2014: 34: 567–575
- Issue published online: 10 MAR 2014
- Article first published online: 2 SEP 2013
- Accepted manuscript online: 5 AUG 2013 12:27AM EST
- Manuscript Accepted: 24 JUL 2013
- Manuscript Received: 7 OCT 2012
- National Natural Science Foundation of China. Grant Numbers: 81030012, 81330010, 81390354, 81170795
- Major National Basic Research Program of P. R. China. Grant Number: 2010CB912504
- American Diabetes Association. Grant Number: #1-13-BS-225
- AMPK ;
- ghrelin receptor;
- gut hormone;
Background & Aims
Ghrelin, a gut hormone with pleiotropic effects, may act as a protective signal in parenchymal cells. We investigated the protective effects of ghrelin on hepatocytes after ischaemia/reperfusion (I/R).
Hepatic injury was assessed by measurement of plasma alanine aminotransferase (ALT) and lactate dehydrogenase (LDH), histological analysis, and TUNEL assay. Effects of exogenous ghrelin and ghrelin receptor gene deletion on I/R induced injury of liver were evaluated.
Ischaemia/reperfusion induced a profound injury to hepatocytes. This was accompanied by elevations in plasma ALT and LDH. Pretreatment with ghrelin significantly reduced elevations in plasma ALT and LDH, and attenuated tissue damage induced by hepatic I/R in mice. Hepatic injury induced by I/R was more pronounced in ghrelin receptor gene null mice. Ghrelin administration blocked the up-regulation of AMP-activated protein kinase (AMPK) activity induced by hepatic I/R.
This study demonstrates that ghrelin contributes to the cytoprotection during hepatic I/R.