Testosterone Deficiency Promotes Hypercholesteremia and Attenuates Cholesterol Liver Uptake via AR/PCSK9/LDLR Pathways

Figure 5

Androgen receptor (AR) antagonist flutamide abolishes the testosterone-induced PCSK9 downregulation and LDLR upregulation while 5α reductase inhibitor dutasteride shows no effect. HepG2 cells were incubated with 0, 30 nM testosterone for 72 h or 30 nM testosterone plus 50 μM AR antagonist flutamide or 1.5 μM 5α reductase inhibitor dutasteride for 72 h. Then cells were harvested. ((a), (b)) PCSK9 and ((c), (d)) LDLR were analyzed by western blotting or real-time quantitative PCR. Data are presented as mean ± SEM. Statistical analyses are one-way ANOVA. ; ; ; ns: non-significant.

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