Shaanxi Key Laboratory of Degradable Biomedical Materials, School of Chemical Engineering, Northwest University, 229 North Taibai Road, Xi'an, Shaanxi 710069, China.
Shaanxi R&D Center of Biomaterials and Fermentation Engineering, School of Chemical Engineering, Northwest University, 229 North Taibai Road, Xi'an, Shaanxi 710069, China.
Food Funct. 2022 Feb 7;13(3):1153-1167. doi: 10.1039/d1fo03026d.
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.
非酒精性脂肪性肝病（NAFLD）是一种代谢性肝病，其病因复杂，被认为是肝细胞癌（HCC）的主要病因之一。由于饮食结构失衡，NAFLD 的发病率呈逐年上升趋势。然而，目前尚无针对 NAFLD 的临床治疗方法。由于其多种药理活性，已对人参皂苷 CK 进行了研究，但它对 NAFLD 的作用及其机制尚不清楚。在本研究中，使用果糖模拟肝脂肪变性，同时使用棕榈酸（PA）和油酸（OA）诱导脂质积累。油红 O 染色评估肝组织和 HepG2 细胞中脂质积累的水平。检测血清和肝生物标志物、western blot 和实时 qPCR 评估肝脂肪变性程度。结果表明，人参皂苷 CK 可减少 HepG2 细胞中的脂质沉积，延缓果糖喂养小鼠体重增加，减轻血清和肝组织中的脂质积累，改善肝炎症和损伤。在机制上，人参皂苷 CK 调节与脂质合成和代谢相关的因子的表达，并激活 LKB1 和 AMPK 的磷酸化。AMPK 的抑制剂 Compound C 部分阻断了人参皂苷 CK 在 HepG2 细胞中的有益作用。总之，人参皂苷 CK 作为 LKB1/AMPK 激动剂，调节脂质代谢，干扰 NAFLD 的进展。
