Abstract
Panax ginseng C.A. Meyer (ginseng) is an edible and traditional medicinal herb, which is reported to have a wide range of biological activity and pharmaceutical properties. There were more studies on ginsenoside and polysaccharides, but fewer on ginseng oligopeptides (GOPs), which are small molecule oligopeptides extracted from ginseng. The present study was designed to investigate the effects and underlying mechanism of ginseng oligopeptide (GOPs) on binge drinking-induced alcohol damage in rats. Sprague Dawley rats were randomly assigned to six groups (n = 10), rats in normal control group and alcohol model group was administered distilled water; rats in four GOPs intervention groups (at a dose of 0.0625, 0.125, 0.25, 0.5 g/kg of body weight, respectively) were administered GOPs once a day for 30 days. Experiment rats were intragastrically administered ethanol at a one-time dose of 7 g/kg of body weight after 30 days. The liver injury was measured through traditional liver enzymes, inflammatory cytokines, expression of oxidative stress markers, and histopathological examination. We found that the GOPs treatment could significantly improve serum alanine aminotransferase and aspartate aminotransferase, plasma lipopolysaccharide, and inflammatory cytokine levels, as well as the oxidative stress markers that were altered by alcohol. Moreover, GOPs treatment inhibited the protein expression of toll-like receptor 4, and repressed the inhibitor kappa Bα and nuclear factor-κB p65 in the liver. These findings suggested that GOPs have a significant protective effect on binge drinking-induced liver injury, and the mechanism possibly mediated by the partial inhibition of lipopolysaccharide—toll-like receptor 4-nuclear factor-κB p65 signaling in the liver.
Highlights
Binge drinking is defined by the National Institute on Alcohol Abuse and Alcoholism (NIAAA)as episodic excessive drinking of alcohol in a short period of time and elevating blood alcohol concentration (BAC) to 0.08% or higher, commonly means consuming more than four or five number of alcoholic beverages on one occasion [1,2]
Most ingested ethanol is metabolized in the liver; excess alcohol consumption is a major cause of preventable liver disease worldwide
In the between present study, we developed the binge drink-Various took into accountofdifferences in alcohol metabolism rodents and humans induced liver injury model in SD rats by gavage 7 g per kg body weight after supplementation with factors cause abnormal lipid accumulation in lipid droplets in the liver, known as hepatic steatosis, ginseng oligopeptides (GOPs) for 30 days
Summary
Alcohol consumption accounts for 6.8% and 2.2% of age-standardized deaths among men and women, with a disproportionate effect on young people [5]. Most ingested ethanol is metabolized in the liver; excess alcohol consumption is a major cause of preventable liver disease worldwide. Many binge drinkers are susceptible to suffer from advanced alcoholic liver diseases (ALD), including a wide spectrum of hepatic lesions, such as fatty liver, hepatic fibrosis, and alcoholic hepatitis [5,6]. Unlike the health issues that are caused by chronic alcoholic consumption have been in-depth researched, less attention has been paid to health effects associated with acute alcoholism; especially liver consequences were often ignored [1,2]. Exploring underlying mechanisms, effective therapy, and agents for protecting alcoholic liver injury is of great importance
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