Hepatoprotective effects of syringin on fulminant hepatic failure induced by D-galactosamine and lipopolysaccharide in mice
Article first published online: 26 APR 2013
Copyright © 2013 John Wiley & Sons, Ltd.
Journal of Applied Toxicology
Volume 34, Issue 3, pages 265–271, March 2014
How to Cite
Gong, X., Zhang, L., Jiang, R., Wang, C.-D., Yin, X.-R. and Wan, J.-Y. (2014), Hepatoprotective effects of syringin on fulminant hepatic failure induced by D-galactosamine and lipopolysaccharide in mice. J. Appl. Toxicol., 34: 265–271. doi: 10.1002/jat.2876
- Issue published online: 27 JAN 2014
- Article first published online: 26 APR 2013
- Manuscript Accepted: 12 FEB 2013
- Manuscript Revised: 30 JAN 2013
- Manuscript Received: 10 DEC 2012
- National Natural Science Foundation of China. Grant Number: No. 81072650
- Natural Science Foundation Project of CQ CSTC. Grant Number: 2010BB5376
- fulminant hepatic failure;
The prognosis for fulminant hepatic failure (FHF) still remains extremely poor with a high mortality and, therefore, better treatments are urgently needed. Syringin, a main active substance isolated from Eleutherococcus senticosus, has been reported to exhibit immunomodulatory and anti-inflammatory properties. In this study, we investigated the effects and underlying mechanisms of syringin on lipopolysaccharide (LPS) and D-galactosamine (D-GalN)-induced FHF in mice. Mice were administered syringin (10, 30 and 100 mg kg–1, respectively) intraperitoneally (i.p) 30 min before LPS/D-GalN then mortality and liver injury were evaluated subsequently. We found that syringin dose-dependently attenuated LPS/D-GalN-induced FHF, as indicated by reduced mortality, inhibited aminotransferase and malondialdehyde (MDA) content, an increased glutathione (GSH) concentration and alleviated pathological liver injury. In addition, syringin inhibited LPS/D-GalN-induced hepatic caspase-3 activation and hepatocellular apoptosis, myeloperoxidase (MPO) activity and intercellular adhesion molecule-1 (ICAM-1) expression, as well as hepatic tissues tumor necrosis factor-alpha (TNF-α) production and NF-κB activation in a dose-dependent manner. These experimental data indicate that syringin might alleviate the FHF induced by LPS/D-GalN through inhibiting NF-κB activation to reduce TNF-α production. Copyright © 2013 John Wiley & Sons, Ltd.