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. Author manuscript; available in PMC: 2017 Aug 1.
Published in final edited form as: Toxicol Appl Pharmacol. 2016 May 12;304:90–98. doi: 10.1016/j.taap.2016.05.007

Fig. 3. PXR participation in MRP2 induction by BZL in HepG2 cells.

Fig. 3

HepG2 cells were transfected with a control non-silencing- (PXR+ cells) or with a PXR specific siRNA (PXR− cells). a. PXR protein levels in cell lysates of PXR+ and PXR− cells were assessed through western blot. PXR O.D. was normalized to GAPDH O.D. Results (mean ± S.D., n = 3) are expressed as percentage of the ratio in PXR+ cells. * different from PXR+, p<0.05. b. To further verify PXR knock-down, CYP3A4 expression was assessed through western blot in PXR+ and PXR− HepG2 cells treated with RIF (20 μM, 24 h) or vehicle (C). CYP3A4 O.D. in control and RIF treated cells was normalized to GAPDH O.D. Results (mean ± S.D., n = 3) are expressed as percentage of the corresponding control. * different from control, p<0.05. c. MRP2 expression was quantified in total lysates of PXR+ and PXR− cells exposed to BZL (200 μM, 24 h) or vehicle (C). MRP2 O.D. was normalized to GAPDH O.D. Results (mean ± S.D., n = 3) are expressed as percentage of the ratio in PXR+ cells. * different from the corresponding control, p<0.05.