Analyses of kamacite, taenite, and plessite from the Welland meteoric iron

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Abstract
Pregnane X receptor (PXR) activation exhibits anti-inflammatory effects via repressing nuclear factor kappa B (NF-κB); however, its over-activation may disrupt homeostasis of various enzymes and transporters. Here, we found that ginsenosides restore PXR/NF-κB signaling in the inflamed conditions without disrupting PXR function in normal conditions. The effects and mechanisms of ginsenosides in regulating PXR/NF-κB signals were determined both in vitro and in vivo. Ginsenosides significantly inhibited NF-κB activation and restored the expression of PXR target genes in TNFα-stimulated LS174T cells. Despite not PXR agonists, ginsenosides repressed NF-κB activation in a PXR-dependent manner. Ginsenosides significantly increased the physical association between PXR and NF-κB p65 subunit and thereby decreasing the nuclear translocation of p65. Ginsenoside Rb1 and compound K (CK) were found to be major bioactive compounds in the regulating PXR/NF-κB signaling. Consistently, ginsenosides significantly attenuated DSS-induced experimental colitis, which was associated with the restored PXR/NF-κB signaling. This study indicates that ginsenosides may elicit anti-inflammatory effects via targeting PXR/NF-κB interaction without disrupting PXR function in healthy conditions. Ginsenoside Rb1 and CK may serve as leading compounds in the discovery of new drugs targeting PXR/NF-κB interaction for IBD therapy.
Reference Key
openalex_W2327026497 Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Jane M Davison
Journal american journal of science
Year 1891
DOI
10.2475/ajs.s3-42.247.64
URL
https://doi.org/10.2475/ajs.s3-42.247.64
Keywords Keywords not found

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