Ginsenoside Rg1 inhibits inflammatory responses via modulation of the nuclear factor‑κB pathway and inhibition of inflammasome activation in alcoholic hepatitis

Int J Mol Med. 2018 Feb;41(2):899-907. doi: 10.3892/ijmm.2017.3297. Epub 2017 Nov 29.


Ginsenoside Rg1 (G‑Rg1) is an active ingredient of Panax ginseng, which has previously been reported to attenuate alcohol‑induced hepatic damage; however, the underlying mechanisms remain largely unknown. The present study aimed to investigate the protective effects of G‑Rg1 on alcohol‑induced cell injury in vitro and on a rat model of alcoholic hepatitis in vivo. For the in vitro model, L‑O2 cells were incubated with ethanol in the presence or absence of G‑Rg1. For the in vivo model, rats were administered ethanol by intragastric injection and were treated with G‑Rg1, or dexamethasone as a control. The results indicated that serum biochemical parameters, including alanine aminotransferase, aspartate aminotransferase and total bilirubin, as well as the expression of nuclear factor (NF)‑κB pathway‑associated inflammatory cytokines, including interleukin (IL)‑6, tumor necrosis factor‑α and IL‑1β, were elevated in response to alcohol; however, they were significantly decreased by G‑Rg1 treatment. Furthermore, NF‑κB pathway activation was reduced by treatment with G‑Rg1. G‑Rg1 also decreased oxidative stress by inhibiting cytochrome P450 2E1 expression and reactive oxygen species production, and promoting glutathione peroxidase expression. Furthermore, G‑Rg1 inhibited the expression levels of caspase‑3 and ‑8, which may be associated with decreased hepatocyte apoptosis. These data suggested that G‑Rg1 may protect hepatocytes against alcohol‑induced injury, through preventing excessive inflammation and hepatocellular apoptosis.

MeSH terms

  • Animals
  • Apoptosis / drug effects
  • Ethanol / toxicity
  • Ginsenosides / administration & dosage*
  • Hepatitis, Alcoholic / drug therapy*
  • Hepatitis, Alcoholic / genetics
  • Hepatitis, Alcoholic / pathology
  • Hepatocytes / drug effects
  • Hepatocytes / pathology
  • Humans
  • Inflammasomes / drug effects
  • Inflammasomes / genetics
  • Inflammation / chemically induced
  • Inflammation / drug therapy*
  • Inflammation / genetics
  • Inflammation / pathology
  • NF-kappa B / genetics
  • Oxidative Stress / drug effects*
  • Rats


  • Ginsenosides
  • Inflammasomes
  • NF-kappa B
  • Ethanol
  • ginsenoside Rg1