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. 2016 Oct;359(1):91–101. doi: 10.1124/jpet.116.234096

Fig. 4.

Fig. 4.

Activation of the PXR attenuates TNFα/IFNγ-induced upregulation of MLCK and inhibits NFκB signaling. (A) Rifaximin (Rifx) attenuates LPS-induced NFκB activation. THP-1-Blue NFκB cells, which express an NFκB-driven SEAP reporter gene, were pretreated with rifaximin (10 μM) for 1 hour prior to exposure to LPS (100 ng/ml). SEAP activity was assessed in the culture supernatant after 16 hours of LPS exposure. ***P < 0.005 compared with control; *P < 0.05 compared with LPS group (n = 4). (B) THP-1-Blue NFκB cells express the PXR (PXR1.1 and PXR1.2 isoforms). (C) Rifaximin attenuates TNFα/IFNγ-induced upregulation of MLCK. Caco-2 monolayers grown for 14 days postconfluence were pretreated with selective rifaximin (10 μM) for 1 hour prior to exposure to TNFα (10 ng/ml) and IFNγ (20 ng/ml) for 16 hours. **P < 0.01 compared with control; #P < 0.05 compared with TNFα/IFNγ (n = 4).