Ginsenoside Rg1, a potential JNK inhibitor, protects against ischemia/reperfusion-induced liver damage. (May 2015)

• Record Type: Journal Article
• Authors: Zhang, Xiao-Jing; He, Chengwei; Li, Peng; Su, Huanxing; Wan, Jian-Bo
• Is Part Of: Journal of functional foods. Volume 15(2015)
• Page Start: 580
• Page End: 592
• Publication Date: 2015-05
• Subjects: ALT alanine amino transferase -- ANOVA a one-way analysis of variance -- AST aspartate amino transferase -- DAPI 4, 6-diamidino-2- phenylindole -- DMEM Dulbecco's modified Eagle's medium -- ERK extracellular signal regulated kinase -- H&E hematoxylin and eosin -- HUVEC human umbilical vein endothelial cells -- H/R hypoxia/reoxygenation -- I/R ischemia/reperfusion -- JNK c-Jun N-terminal kinase -- LDH lactate dehydrogenase -- LPS lipopolysaccharides -- MAPK mitogen-activated protein kinases -- TUNEL terminal deoxynucleotidyl transferase dUTP nick end labeling; Ginsenoside Rg1 -- Hepatic ischemia/reperfusion -- Inflammation -- Apoptosis -- JNK signaling; Ginsenoside Rg1 (PubChem CID: 441923); Functional foods -- Analysis -- Periodicals; Food -- Biotechnology -- Periodicals; Nutrition -- Periodicals; 613.2
• DOI: 10.1016/j.jff.2015.04.010
• Languages: English
• ISSNs: 1756-4646

Abstract

Highlights: There is no effective approach to prevent hepatic I/R-induced liver damage. Ginsenoside Rg1 retards hepatic I/R injury via inhibiting inflammation and apoptosis. The hepatoprotection of ginsenoside Rg1 is associated with blockage of JNK signaling. Abstract: 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.