Journal
JOURNAL OF FUNCTIONAL FOODS
Volume 15, Issue -, Pages 580-592Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.jff.2015.04.010
Keywords
Ginsenoside Rg1; Hepatic ischemia/reperfusion; Inflammation; Apoptosis; JNK signaling
Categories
Funding
- Research Committee of the University of Macau [MYRG123-ICMS12, MYRG111-ICMS13]
- Macao Science and Technology Development Fund [010/2013/A1]
Ask authors/readers for more resources
Hepatic ischemia/reperfusion (I/R), characterized by severe inflammation and cell death, causes significant liver damage, and there are no effective approaches to prevent this pathological condition. We evaluated the potentially protective functions of ginsenoside Rg1 in hepatic I/R injury and the underlying mechanisms. A mouse hepatic I/R model was established by 60 min of induced ischemia followed by 0, 6, 12 or 24 h of reperfusion. Ginsenoside Rg1 (20 mg/kg/day) significantly promoted hepatic function and suppressed liver necrosis and inflammatory responses. Mechanistically, the JNK/MAPK signaling was dramatically diminished by ginsenoside Rg1. Furthermore, we unexpectedly found that only the cytotoxicity induced by inflammation, rather than oxidative stress, was significantly inhibited by ginsenoside Rg1 in vitro, and this inhibition was almost completely abolished by treatment with a specific JNK activator, anisomycin. Thus, ginsenoside Rg1 exerts protective effects against hepatic I/R in a JNK signaling-dependent manner. (C) 2015 Elsevier Ltd. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available