Notoginsenoside R1 Attenuates Experimental Inflammatory Bowel Disease via Pregnane X Receptor Activation

@article{Zhang2015NotoginsenosideRA,
  title={Notoginsenoside R1 Attenuates Experimental Inflammatory Bowel Disease via Pregnane X Receptor Activation},
  author={Jing-jing Zhang and Lili Ding and Baocan Wang and Gaiyan Ren and Aning Sun and Chao Deng and Xiaohui Wei and Sridhar Mani and Zhengtao Wang and Wei Dou},
  journal={The Journal of Pharmacology and Experimental Therapeutics},
  year={2015},
  volume={352},
  pages={315 - 324},
  url={https://api.semanticscholar.org/CorpusID:8180670}
}
R1 attenuates experimental IBD possibly via the activation of intestinal PXR signaling, and the anti-inflammatory effect of R1 was confirmed in trinitrobenzene sulfonic acid–induced colitis in mice.
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43 References

Chrysin Ameliorates Chemically Induced Colitis in the Mouse through Modulation of a PXR/NF-κB Signaling Pathway

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Pregnane X receptor as a target for treatment of inflammatory bowel disorders.

Alleviation of Gut Inflammation by Cdx2/Pxr Pathway in a Mouse Model of Chemical Colitis

Pregnane X Receptor (PXR), a master regulator of drug metabolism and inflammation, is abundantly expressed in the gastrointestinal tract and pharmacological targeting of intestinal PXR using natural metabolically labile ligands could serve as effective and potent therapeutics for gut inflammation that avert systemic drug interactions.

Pregnane-X-receptor mediates the anti-inflammatory activities of rifaximin on detoxification pathways in intestinal epithelial cells.

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Preadministration of rifaximin ameliorated the clinical hallmarks of colitis in DSS- and TNBS-treated hPXR mice as determined by body weight loss and assessment of diarrhea, rectal bleeding, colon length, and histology, suggesting that human PXR may be an effective target for the treatment of IBD.

Pregnane X receptor activation ameliorates DSS-induced inflammatory bowel disease via inhibition of NF-kappaB target gene expression.

The data suggest that P XR-mediated repression of NF-kappaB target genes in the colon is a critical mechanism by which PXR activation decreases the susceptibility of mice to DSS-induced IBD.

Panax notoginseng saponins attenuate atherosclerosis via reciprocal regulation of lipid metabolism and inflammation by inducing liver X receptor alpha expression.

Chrysin, a natural flavone, improves murine inflammatory bowel diseases.

Paeoniflorin abrogates DSS-induced colitis via a TLR4-dependent pathway.

For the first time, the present study indicates that paeoniflorin abrogates DSS-induced colitis via decreasing the expression of TLR4 and suppressing the activation of NF-κB and MAPK pathways.

Loss of detoxification in inflammatory bowel disease: dysregulation of pregnane X receptor target genes.

Dysregulation of xenobiotic metabolism and PXR activity in the gut is likely to contribute to the pathophysiology of UC.