Figure 2
E2 increased the lipid secretion levels and HMGCR expression in HepG2 cells in a dose-dependent manner, effects attenuated in the presence of ICI, an ER antagonist.
(a) The secretion levels of TC and LDL-C in HepG2 cells after 24 hours treatment with different doses of E2, or co-treatment with E2 and ER antagonist ICI (10−5 mol/L). (b) The LPL, LCAT and CYP7A1 mRNA expression in HepG2 cells after 24 hours treatment with E2 in a dose-dependent manner. (c) The HMGCR mRNA expression in HepG2 cells after 24 hours treatment with E2 in a dose-dependent manner or co-treatment with E2 and ICI (10−5 mol/L). (d) The HMGCR protein expression in HepG2 cells after 24 hours treatment with E2 in a dose-dependent manner. The experiments were repeated three times and data were presented as Mean ± SEM. *P < 0.05 and **P < 0.01 compared with the corresponding control group, respectively. #P < 0.05 and ##P < 0.01 compared with the value in the E2-treated group, respectively. E2: estradiol; TC: total cholesterol; LDL-C: low-density lipoprotein cholesterol; ICI: ICI 182,780; ER: estrogen receptor; LPL: lipoprotein lipase; LCAT: lecithin cholesterol acyl transferase; CYP7A1: cholesterol 7α-hydroxylase; HMGCR: 3-hydroxy-3-methylglutaryl-CoA reductase.
