Ginsenoside CK ameliorates hepatic lipid accumulation activating the LKB1/AMPK pathway and .

Nonalcoholic fatty liver disease (NAFLD) is a metabolic liver disease with a complex etiology, and is considered as one of the main causes of hepatocellular carcinoma (HCC). The incidence of NAFLD has presented an increasing trend annually as a result of disequilibrium in the dietary structure. However, no specific treatment has been approved for clinical therapy in NAFLD. Ginsenoside CK has been investigated given its various pharmacological activities, but its effects against NAFLD and the underlying mechanism are still unclear. In this study, fructose was used to simulate hepatic fatty degeneration , while palmitic acid (PA) and oleic acid (OA) were applied to induce lipid accumulation . The level of lipid accumulation in hepatic tissue and HepG2 cells was evaluated by Oil Red O staining. Detection of serum and liver biomarkers, western blotting, and real-time qPCR were conducted to assess the degree of hepatic steatosis. Our results indicated that ginsenoside CK could decrease the lipid deposition in HepG2 cells, retard the increase of body weight of fructose-fed mice, alleviate the lipid accumulation in serum and hepatic tissue and improve the hepatic inflammation and injury. Mechanically, ginsenoside CK modulated the expression of factors correlated with lipid synthesis and metabolism and activating the phosphorylation of LKB1 and AMPK. Compound C, an inhibitor of AMPK, partially abrogated the beneficial effects of ginsenoside CK in HepG2 cells. In summary, ginsenoside CK acts as a LKB1/AMPK agonist to regulate the lipid metabolism and interfere with the progression of NAFLD.