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Transducer Mechanism: Nuclear Receptors

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Adrenergic Antagonists: Chemistry and Classification of ɑ-Receptor Blockers01:17

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Dose-Response Relationship: Selectivity and Specificity01:25

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Related Experiment Video

Updated: Jun 21, 2026

Methods for the Discovery of Novel Compounds Modulating a Gamma-Aminobutyric Acid Receptor Type A Neurotransmission
07:16

Methods for the Discovery of Novel Compounds Modulating a Gamma-Aminobutyric Acid Receptor Type A Neurotransmission

Published on: August 16, 2018

Oleanolic acid is a selective farnesoid X receptor modulator.

Wenming Liu1, Chiwai Wong

  • 1University of Science and Technology of China, Hefei, China.

Phytotherapy Research : PTR
|August 5, 2009
PubMed
Summary

Oleanolic acid (OA) acts as a gene-selective modulator of the farnesoid X receptor (FXR). This traditional Chinese medicine ingredient selectively impacts FXR target genes, offering potential therapeutic benefits for liver conditions.

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Last Updated: Jun 21, 2026

Methods for the Discovery of Novel Compounds Modulating a Gamma-Aminobutyric Acid Receptor Type A Neurotransmission
07:16

Methods for the Discovery of Novel Compounds Modulating a Gamma-Aminobutyric Acid Receptor Type A Neurotransmission

Published on: August 16, 2018

Area of Science:

  • Pharmacology
  • Hepatology
  • Molecular Biology

Background:

  • Oleanolic acid (OA) is a component of Traditional Chinese Medicine used for liver ailments.
  • The farnesoid X receptor (FXR) is a key regulator of bile acid metabolism in the liver.
  • OA's potential mechanism of action through FXR was investigated.

Purpose of the Study:

  • To determine if Oleanolic acid (OA) interacts with the farnesoid X receptor (FXR).
  • To elucidate the effect of OA on FXR activity and its downstream target genes.
  • To assess OA's potential as a selective FXR modulator.

Main Methods:

  • In vitro binding assays to assess OA interaction with FXR's ligand binding domain (LBD).
  • Reporter gene assays to measure FXR-LBD activity modulated by OA and chenodoxycholic acid (CDCA).
  • Quantitative analysis of FXR target gene expression (BSEP, OST-beta, SHP) following OA treatment.

Main Results:

  • OA directly binds to the FXR LBD and inhibits coactivator recruitment (SRC-3).
  • OA dose-dependently suppresses CDCA-induced FXR-LBD activity.
  • OA selectively modulates FXR target genes, partially inhibiting BSEP, not affecting OST-beta, and enhancing SHP expression.

Conclusions:

  • Oleanolic acid functions as a gene-selective modulator of FXR.
  • OA's distinct effects on FXR target genes suggest a novel therapeutic mechanism for liver diseases.
  • Further research into OA's selective FXR modulation could yield new treatments for hepatic conditions.