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Activation of PXR inhibits LPS-induced NF-κB activation by increasing IκBα expression in HepG2 cells
Nanhui Ye,Hang Wang,Qiaoling Li,Chaotong Lin,Huahua Feng,Suying Lin,Jing Hong,Chunn Meng 대한독성 유전단백체 학회 2018 Molecular & cellular toxicology Vol.14 No.1
A limited number of xenobiotic-induced inflammatory episodes occur in the human liver and small intestine under normal physiological conditions, although many xenobiotic agents are metabolized in these organs every day. In this study, we found that rifampicin-activated pregnane X receptor (PXR) plays an important role in the suppression of lipopolysaccharide-activated nuclear factor kappa B (NF-κB) activity by increasing the expression of the inhibitor of κBα (IκBα) in HepG2 cells. Rifampicin did not increase the expression of IκBα in PXR knockdown HepG2 cells. Furthermore, we found that the activation of PXR could inhibit the lipopolysaccharide-stimulated nuclear translocation of NF-κB p50/p65 using electrophoretic mobility shift assay, immunoprecipitation assays, and microscopy. High levels of IκBα directly interacted with NF-κB and prevented its nuclear translocation, thus inhibiting its binding to consensus DNA sequences in nuclei. Xenobiotic-activated tissue-specific PXR might exert anti-inflammatory actions by antagonizing the xenobiotic-induced transcriptional activity of NFκB in the liver and small intestine. The results also showed that activation of PXR arrested the HepG2 cell cycle in the G0/G1 phase and exhibited cancer prevention potential by inhibiting inflammatory reactions in cells.
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