Objective: To explore the therapeutic effect of Sedum emarginatum (SE) and its polysaccharide on alcoholic liver disease. Methods: First, we ground fresh SE to obtain homogenate, and then test the effect of SE on a mouse model of acute alcoholic fatty liver disease (AFLD). Kunming female mice were given intragastric administration of alcohol once every 12 hours to induce AFLD, three times in total, and the mice received ethanol and SE at the same time. The mice were sacrificed 4 hours after the last alcohol administration, and serum and liver were collected for testing. We found that SE was effective and then carried out subsequent experiments. The dried SE powder was extracted under heating and reflux by different polar solvents: petroleum ether, ethyl acetate, methanol and water. The extracting solution were heat and concentrated to obtain an extract. The water part was purified to obtain polysaccharide. We tested the therapeutic effect of each part of SE in a mouse model of early alcoholic hepatitis (AH). Mice were given 5 g/kg of alcohol every 12 hours, a total of 9 times, and lipopolysaccharide (LPS) was injected intraperitoneally at the 36 h and 84 h. After 4 hours of the last gavage, the mice were sacrificed. The serum and liver tissue were used to tested relevant biochemical indexes. Results: SE had a certain reversal effect on the increase of serum triglycerides caused by alcohol, and it had a better effect on the accumulation of lipid droplets in liver tissues. Oil red O staining proved this result. In the second acute experiment, the mortality rate of the animal in the model group was 7/12, and the mortality rate in each treatment group was 1/8, 1/7, 4/8, and 1/8. In all parts, the crude polysaccharide did not significantly reverse the increase of serum triglyceride levels in early AH, but it could significantly alleviate the increase of inflammatory foci and steatosis in liver tissue. The transmission electron microscopy result indicates that the crude polysaccharide component has a certain protective effect on mitochondrial damage caused by alcohol. Conclusion: SE can reduce fatty liver and hyperlipidemia caused by alcohol, and its polysaccharide can reduce liver inflammation in the early alcoholic hepatitis by protecting mitochondron.
A Novel Mouse Model of Acute‐on‐Chronic Cholestatic Alcoholic Liver Disease: A Systems Biology Comparison With Human Alcoholic Hepatitis
