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. 2011 Dec 13;93(4):674–681. doi: 10.1093/cvr/cvr330

Figure 6.

Figure 6

PXR activation induces GST activity (n = 5), GPx activity (n = 6), and GSTM1 mRNA expression (n = 6) in RASMC treated with PCN (10 μmol/L 24 h) (A). Data represent fold change in enzyme activity or GSTM1:GAPDH ratio for real-time PCR from vehicle (0.1% DMSO)-treated cells ±SE. (B and C) PXR activation (10 μmol/L PCN, 24 h) protects RASMC from hydrogen peroxide (1 mmol/L, 3 h post-PCN)-induced cell death. (B) Representative photomicrographs of RASMC morphology post-treatment. Magnification ×100. Scale bar represents 200 μm. (C) Data represent viability as a percentage of control ±SE (n = 5 triplicate samples). (D) Expression of PXR-DN prevents PXR activator-mediated protection of RASMC viability. RASMC transfected with control vector (pcDNA 3.1) or PXR-DN plasmid in the presence of GFP expression vector (pEGFPN-1) at a ratio of 9:1 were treated 24 h post-transfection with 10 μmol/L PCN for 24 h and then 1 mmol/L hydrogen peroxide for 3 h before GFP cells were counted by fluorescent microscopy. Data represent the mean from three (×200) magnification fields per triplicate, from n = 3 experiments ±SE. (A) *P < 0.05 vs. vehicle determined by one-sample t-test. (C) *P < 0.05, (A) **P < 0.01 vs. control/vehicle determined by paired Student's t-test. (D) *P < 0.05, ***P < 0.001 determined by two-way ANOVA with Bonferroni's post hoc test.