Protective effects of ginsenoside Rk3 against chronic alcohol-induced liver injury in mice through inhibition of inflammation, oxidative stress, and apoptosis

Alcoholic liver disease (ALD), as one of the most common diseases, has become a global threat to human health. The aim of this study was designed to investigate the hepatoprotective effects of ginsenoside Rk3 against ALD and to discover the potential mechanisms of these protective effects. Mice were intragastrically administered 50% alcohol and treated with ginsenoside Rk3 (25 and 50 mg/kg) once per day for 6 weeks. The results indicated that ginsenoside Rk3 promoted hepatic function through significant downgrading AST and ALT levels in the serum, attenuating oxidative stress, and restoring antioxidant balance in hepatic tissue. Additionally, ginsenoside Rk3 significantly reduced the expression of inflammatory cytokines, such as NF-κB, TNF-α, IL-6, and IL-1β in the mice. Furthermore, ginsenoside Rk3 supplementation significantly inhibited apoptotic protein expression in the liver. The present study clearly demonstrates that ginsenoside Rk3 exerts a protective effect against ALD-induced liver injury because of its antioxidant, anti-apoptotic, and anti-inflammatory activities. The findings from the present investigation show that ginsenoside Rk3 might be a promising candidate treatment agent against ALD. [Display omitted] •Ginsenoside Rk3 prevented liver injury induced by binge ethanol.•Ginsenoside Rk3 ameliorated the inflammation and oxidative stress under the condition of chronic ethanol exposure.•Ginsenoside Rk3 inhibited the apoptosis induced by ethanol partially through caspase pathways.