SGL 121 Attenuates Nonalcoholic Fatty Liver Disease through Adjusting Lipid Metabolism Through AMPK Signaling Pathway

Figures

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  Figure 1. Effects of SGL 121(ginsenoside F2-enhanced mixture) on body weight and fat mass in nonalcoholic fatty liver disease (NAFLD)-induced mice. (A) Bodyweight changes, (B) bodyweight at week 12, (C) dual-energy X-ray absorptiometry (DXA) image of fat distribution, and (D) fat mass. Data are presented as the mean ± SE, n = 8. * p < 0.05, ** p < 0.01, and *** p < 0.001 compared to the high-fat, high-carbohydrate (HFHC) group.

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  Figure 2. Effect of SGL 121 on lipid accumulation in NAFLD-induced mice. (A) Oil red O or hematoxylin staining of the liver, (B) hepatic triglyceride (TG), (C) hepatic total cholesterol (TC), (D) serum TG, (E) serum TC, (F) high-density lipoprotein (HDL) cholesterol, and (G) low-density lipoprotein (LDL) cholesterol levels. Data are presented as the mean ± SE, n = 8. * p < 0.05, ** p < 0.01, and *** p < 0.001 compared to the HFHC group.

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  Figure 3. Effect of SGL 121 on liver function improvement in NAFLD-induced mice. (A) Serum aspartate aminotransferase (AST) activity, (B) serum AST activity, (C) serum γ-glutamyl transpeptidase (GGT) activity, and (D) malondialdehyde (MDA) level in liver. Data are presented as the mean ± SE, n = 8. * p < 0.05, ** p < 0.01, and *** p < 0.001 compared to the HFHC group.

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  Figure 4. Effects of SGL 121 on hepatic lipid gene expression in NAFLD-induced mice. (A) sterol regulatory element-binding protein-1 (SREBP-1) mRNA levels, (B) fatty acid synthase (FAS) mRNA levels, (C) SREBP-1 and FAS protein expression levels. The graph indicates the expression level against β-actin expression level. Data are presented as the mean ± SE, n = 8. * p < 0.05 and ** p < 0.01 compared to the HFHC group.

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  Figure 5. Antioxidant activities of SGL 121 on various radicals determined by (A) 2,2-diphenyl-1-picrylhydrazyl (DPPH) radical scavenging activity and (B) superoxide dismutase (SOD) radical scavenging activity. Vitamin C (A) and trolox (B) were used as positive controls. Data are presented as the mean ± SD. * p < 0.05, ** p < 0.01, and *** p < 0.001 compared to the control.

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  Figure 6. Effects of SGL 121 on tert-butyl hydroperoxide (t-BHP)-induced (A) cytotoxicity, (B) hepatotoxicity, (C) inhibition of reactive oxygen species (ROS) production, and (D) antioxidant enzymes. Data are presented as the mean ± SD. ## p < 0.01 and ### p < 0.001 compared to the control. ** p < 0.01 and *** p < 0.001 compared to t-BHP treatment alone.

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  Figure 7. Effects of SGL 121 on HO-1 expression and Nrf2 nuclear translocation in HepG2 Cells. (A) Time-course analysis of mRNA and protein expression of HO-1 at 100 µg/mL SGL 121, (B) analysis of mRNA and protein expression of HO-1 after 6 h treatment of 25, 50, and 100 µg/mL SGL 121, (C) time course analysis of Nrf2 levels in nuclear and cytosolic extracts at 100 µg/mL SGL 121, and (D) analysis of Nrf2 levels in nuclear and cytosolic extracts after 25, 50, and 100 µg/mL SGL 121 treatment for 6 h. Data are presented as the mean ± SD. * p < 0.05, ** p < 0.01 and *** p < 0.001 compared to the control.

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  Figure 8. Effects of SGL 121 on lipid accumulation and lipogenesis in HepG2 Cells. (A) Lipid accumulation of Oil red O contents was quantified by spectrophotometric analysis, (B) relative mRNA levels of SREBP-1, FAS, acetyl CoA carboxylase (ACC), and peroxisome proliferator-activated receptor α (PPARα) were assayed by real-time PCR analysis, and (C) protein expression of p-adenosine monophosphate-activated protein kinase (AMPK), AMPK, SREBP-1, FAS, p-ACC, ACC, and PPARα was determined by Western blotting. The graph indicates the expression level against β-actin expression level. Data are presented as the mean ± SD. ## p < 0.01 and ### p < 0.001 compared to the control. * p < 0.05, ** p < 0.01 and *** p < 0.001 compared to free fatty acids (FFA) treatment alone.