Ginsenoside Rg1, a potential JNK inhibitor, protects against ischemia/reperfusion-induced liver damage

Journal of Functional Foods

Jian-Bo Wan¹  Xiao-Jing Zhang²  Huanxing Su²  Peng Li²  Chengwei He² 

[1] Corresponding author. Institute of Chinese Medical Sciences, University of Macau, Taipa, Macao, China. Tel.: [phone];State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao, China;

关键词: Ginsenoside Rg1;    Hepatic ischemia/reperfusion;    Inflammation;    Apoptosis;    JNK signaling;   

DOI  :  

来源: DOAJ

【 摘 要 】

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.

【 授权许可】

Unknown