Korean Red Ginseng Extract Suppresses the Progression of Alcoholic Fatty Liver in a Rat Model

Abstract

Alcoholic fatty liver (AFL) is the most common liver disease among Korean men, and Korean red ginseng has been used as a folk medicine to diverse diseases in Korea. Therefore, we examined if Korean red ginseng extract (KRG) could be a suppressive agent on AFL in a rat model or not. Experimental rats were fed the Lieber DeCarli diet with 36% of energy intake from ethanol, and divided into three groups which daily co-administered KRG 0, 700 and 1400 mg/kg for six weeks, respectively. Naive rats were fed iso-caloric control diet without ethanol and KRG. We investigated histopathological hepatic characteristics, hepatic and plasma lipid concentrations, hepatic hydroxyproline contents, heart/liver radioactivity ratio of 201 Thallium and liver/body weight of the rats at the end point. Ethanol intake brought about steatotic, inflammatory, necrotic and fibrotic changes of livers significantly, and it also lead the rats to increase hepatic triglyceride and hydroxyproline contents, plasma total cholesterol and low density lipoprotein cholesterol levels, and liver/body weight. However, co-administration of KRG 1400 mg/kg suppressed fat accumulation and fibrotic initiation in AFL rat model significantly. It was also inclined to attenuate inflammatory cell infiltration, hydroxyproline accumulation, and increasing liver/body weight, even though plasma lipid levels and heart/liver ratios were not successfully improved by six-week-long intakes of KRG. In conclusions, co-administration of KRG 1400 mg/kg could significantly suppress steatosis in AFL rat model, and it might need longer ingestion of KRG than six weeks to improve plasma lipid imbalance.

Influence of Omega-3 and Green Tea Extract on Alcohol-Induced Liver Injury in Rats

“…The marked fatty changes in the hepatic tissue correlated with the abnormal biochemical parameters observed in the present study. Steatosis; accumulation of lipids in the hepatocytes, is the most striking initial manifestation of alcohol-induced liver injury which are highly sensitive to further alcoholic insult leading to the development of more severe manifestations of alcohol-induced liver diseases such as hepatitis, fibrosis, cirrhosis and eventually hepatocellular carcinoma [50]. Upregulation of sterol regulatory element-binding protein (SREBP)-1c is one of the mechanisms in the development of steatosis [57].…”