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. 2016 May 9;7:120. doi: 10.3389/fphar.2016.00120

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Copyright © 2016 Esposito, Nobile, Gigli, Seguella, Pesce, d’Alessandro, Bruzzese, Capoccia, Steardo, Cuomo and Sarnelli.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Rifaximin (0.1, 1.0, and 10 μM) down-regulates the TLR4/MyD88/NF-κB pathway by a PXR-dependent mechanism. (A) Immunoblot showing the TLR4, MyD88, and phosphorylated/unphosphorylated TAK1 protein bands, and (B) Relative densitometric analysis of immunoreactive bands (arbitrary units normalized against the expression of the housekeeping GAPDH protein) showing the effects of rifaximin, given alone or in the presence of ketoconazole (10 μM), on the expression of TLR4, MyD88, and pTAK1 in Caco-2 cell line. (C) EMSA analysis showing concentration-dependent inhibition of NF-κB activation by rifaximin, and (D) Relative densitometric analysis of NF-κB bands. Results are expressed as mean ± SEM of n = 5 experiments performed in triplicate. ^∗∗∗p < 0.001 vs. vehicle group; ^∘∘∘p < 0.001, ^∘∘p < 0.01 and °p < 0.05 vs. TcdA group.