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

Abstract

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.