Tripterygium regelii decreases the biosynthesis of triacylglycerol and cholesterol in HepG2 cells

Figures & data

Fig. 1. UPLC-PDA-QTOF-MS chromatograms of TR: 3-O-[α-D-arabinopyranosyl-(1→6)-β-D-glucopyranosyl]quercetin (1), 3-O-β-rutinosylquercetin (2), 3-O-β-D-galactopyranosylquercetin (3), 3-O-β-D-glucopyranosylquercetin (4) and celastrol (5).

Fig. 2. Effect of TR-LM on intracellular neutral lipid and cholesterol contents in HepG2 cells.

Notes: (A) Cells were treated with various concentrations (12.5, 25, 50 and 100 μg/mL) for 24 h. Then, neutral lipids detected by using Bodipy 493/503, and cholesterols stained by cholesterol-sequestering agent Filipin lll. The counter staining of nucleus was performed with Hoechst 33342. (B) Fluorescence of Bodipy 493/503 was quantified by flow cytometry at FITC channel. (C) Total cholesterol quantification assay was carried out by manufacturer’s instructions. The bar graphs are presented as mean ± S.D. (n = 2). Significance: **p < 0.01 vs. control.

Fig. 3. Effect of TR-LM on transcriptional and translational expression of lipid metabolism-associated genes in HepG2 cells.

Notes: Cells were incubated with indicated concentrations of TR-LM and incubated for 2 h. RT-PCR and western blot were carried out to analysis of the genes expression related to lipogenesis (A and B), cholesterogenesis (C and D), and lipolysis (E and F).

Fig. 4. TR-LM blocks de novo TG and cholesterol synthesis.

Notes: (A) Lipid profile analyzed by using TLC after treatment of [¹⁴C] acetate as radiolabeled substrate. Relative percentage of newly synthesized [¹⁴C] TG was shown as a graph. C75 (15 μg/mL), a FAS inhibitor, was used as a positive control. (B) In vitro HMG-CoA reductase activity. Pravastatin, a specific HMG-CoA reductase inhibitor (500 nM), was used as apositive control. Data are presented as mean ± S.D. (n = 3). Significance: *p < 0.05; **p < 0.01 vs. control.