Modulatory effects of Acanthopanax koreanum Nakai on oxidative stress induced by combination of alcohol and high‐fat diet in C57BL/6j mice.

Abstract

Excess alcohol consumption is liked to a high risk of liver problem, which can develop into steatohepatitis and liver cirrhosis in modern society. A high‐fat (HF) diet can also lead to the progression of fatty liver. Therefore the role of alcohol as a risk factor for liver damage may be clearly demonstrated by a combination of both alcohol and HF diet. We tested this hypothesis by using Acanthopanax koreanum Nakai (AK) as a model compound. C57BL/6j mice (8‐week‐old; n=56) were randomly divided into seven groups for four weeks; normal control (NC), ethanol control (EC), EC + high fat diet (EF), EC + 1% AK (ECL), EC + 3% AK (ECH), EF + 1% AK (EFL), and EF + 3% AK (EFH). AK was provided in the diet and 50% (v/v) ethanol was provided by gavage. ADH had no significant difference among all groups. Hepatic ALDH activities were significantly increased in the EH compared with the NC, whereas the ECH showed a tendency of increase in ALDH activity compared with the EC. CYP2E1 was significantly increased in both the EC and the EF compared with the NC. ECH tended to decrease CYP2E1 protein expression compared with the EC and the EFL and EFH showed a tendency to decrease compared with the EF. Peroxisomal catalase (CAT) and glutathione reductase (GR) had a tendency to decrease in the EC; CAT and GR decreased significantly in the HF than in the NC. The AK treatment groups (ECH and EFH) showed a tendency to increase in CAT and GR. Taken together, the results support the hypothesis that combination of alcohol and high‐fat diet provide better animal model for testing the alcohol‐induced oxidative stress. Based on this animal model, the results suggest that AK administration in particularly at a high dose may have protective effects against hepatic injury via anti‐oxidative function.