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. 2019 Jan 8;9:3257. doi: 10.3389/fmicb.2018.03257

Figure 3.

Figure 3

The anti-HBV activity of troglitazone is not mediated via PPARγ activity. (A–C) HepG2-hNTCP-C4 cells were transfected with a reporter plasmid carrying binding elements for PPAR (PPRE) together with expression plasmids encoding PPARγ and RXRα (A). The cells were treated with or without 25 μM troglitazone, 25 μM pioglitazone (B), or 25 μM troglitazone in the presence or absence of 1 mM SR-202, a PPARγ antagonist, for 24 h (C), and luciferase reporter activity was measured. (D,E) HepG2-hNTCP-C4 cells treated with or without 25 μM troglitazone, 25 μM pioglitazone (D), or 25 μM troglitazone in the presence or absence of 1 mM SR-202 (E) were subjected to the HBV infection assay according to the scheme shown in Figure 1B. HBV infection was evaluated by quantifying HBs antigen in the culture supernatant. Data are shown as mean ± SD. Statistical significance was determined using a two-tailed non-paired Student's t-test (N.S.; not significant, **P < 0.01).