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Chinese Journal of Experimental Traditional Medical Formulae ; (24): 100-106, 2020.
Article in Chinese | WPRIM | ID: wpr-873159

ABSTRACT

Objective:To investigate the effect and mechanism of ginsenoside Rg1(G-Rg1)in ameliorating lipid uptake and oxidation in HepG2 cells induced by free fatty acids (FFA). Method:HepG2 cells were divided into normal group, model group,low-dose ginsenoside Rg1 group (25 μmol·L-1) and high-dose G-Rg1 group (50 μmol·L-1). HepG2 cells were treated with 1 mmol·L-1 free fatty acid for 24 h to construct the NAFLD cell model, and then treated with 25,50 μmol·L-1 G-Rg1 for 24 h. The effect of G-Rg1 on HepG2 cell activity was determined by cell counting kit-8(CCK-8) assay. The level of triglyceride (TG) was detected by micro method. The accumulation of lipid droplets was observed by oil red O staining. Quantitative real-time fluorescence polymerase chain reaction (Real-time PCR) and Western blot were used to detect the alterations of key genes and proteins relating to lipid uptake and metabolism. Result:Compared with the normal group, the intracellular TG level and the absorbance of the oil red O staining in the model group were significantly increased (P<0.01). Compared with the model group, G-Rg1 reduced TG and lipid deposition were significantly reduced (P<0.01).Results of Real-time PCR and Western blot showed that compared with normal group, model group peroxisome proliferators-activated receptors gamma(PPARγ),fatty acid binding protein 1(FABP1),fatty acid transport protein 2/5(FATP2/5)and fatty acid translocase(CD36)expressions increased(P<0.05),whereas peroxisome proliferators-activated receptors α(PPARα),carnitine palmitoyltransferase 1(CPT1)and peroxisomal acyl-coenzyme A oxidase 1(ACOX1)expressions decreased(P<0.05). Compared with the model group, the expressions of PPARγ, FABP1, FATP2, FATP5 and CD36 in the G-Rg1 group were decreased (P<0.05,P<0.01), while the expressions of PPARα, CPT1 and ACOX1 were increased (P<0.05,P<0.01). Conclusion:G-Rg1 can ameliorate lipid deposition in NAFLD cell model by reducing lipid uptake and increasing lipid oxidation.

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