We studied the effects of Akebia quinata fruit extract (AQ) on acute alcohol-induced hepatotoxicity in mice. AQ (30-1,000 mg/kg body weight (BW) per day) was orally administered to the study group, once daily for 1 week. On the last day of AQ treatment, ethanol (6 mg/kg BW) was orally administered to induce acute liver injury. The AQ-treated group showed significantly lower levels of alanine aminotransferase and aspartate aminotransferase, compared to the only ethanol-treated group (ETG). The glutathione level in the AQ-treated group elevated up to 20.6%, compared to that observed in the ETG. The mRNA expression of glutathione synthetic enzymes was also higher in the AQ-treated group, compared to the ETG. The AQ-treated group also exhibited lower levels of expression of NADPH oxidase 4 and tumor necrosis factor alpha mRNA. Thus, these results show that AQ treatment can be a potential method to reduce oxidative stress and inflammation in ethanol-treated mouse liver and also that AQ can be a useful therapeutic agent for acute alcohol-induced hepatotoxicity.
- Acute alcohol-induced liver injury
- Akebia quinata
- NADPH oxidase 4
- Tumor necrosis factor alpha