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Panaxytriol upregulates CYP3A4 expression through the interaction between nuclear regulators and DNA response

Jingdi Yan1, Qi Gu2, Chao Meng2

  • 1Clinical Pharmacology Institute, Pharmaceutical School, Nanchang University, Nanchang, 330031, PR China; Department of Pharmacy, The Second Affiliated Hospital of Nanchang University, Nanchang, 330006, PR China.

Journal of Ethnopharmacology
|March 22, 2023
PubMed
Summary

Panaxytriol enhances cytochrome P3A4 (CYP3A4) expression by promoting pregnane X receptor (PXR) binding to coactivators and DNA elements. This study reveals an interactive regulatory mechanism between PXR and constitutive androstane receptor (CAR).

Keywords:
CYP3A4DNA response elementsInteractive dialogueNuclear receptorsNuclear regulatorsPanaxytriol

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Area of Science:

  • Pharmacology
  • Molecular Biology
  • Natural Products Chemistry

Background:

  • Cytochrome P3A4 (CYP3A4) is a key drug-metabolizing enzyme.
  • Pregnane X receptor (PXR) and constitutive androstane receptor (CAR) are critical regulators of CYP3A4 expression.
  • Panaxytriol, from Panax ginseng, induces CYP3A4 via PXR, but its mechanism is unclear, especially concerning CAR antagonism.

Purpose of the Study:

  • To elucidate the mechanism by which panaxytriol induces CYP3A4 expression.
  • To investigate the interactions between nuclear regulators (PXR, CAR) and DNA response elements.
  • To understand the role of coactivators SRC-1 and P300 in this process.

Main Methods:

  • Immunoprecipitation assays were used to determine the binding of PXR and CAR with coactivators SRC-1 and P300 in HepG2 and Huh-7 cells.
  • Chromatin immunoprecipitation assays were employed to analyze PXR and CAR interactions with the CYP3A4 promoter response elements ER-6/DR-3.
  • CAR silencing was performed to assess its role.

Main Results:

  • Panaxytriol increased the binding of PXR to SRC-1, P300, and the ER-6/DR-3 elements in a dose-dependent manner.
  • CAR silencing further enhanced PXR binding.
  • CAR binding to SRC-1 and ER-6/DR-3 elements increased at high panaxytriol concentrations, but CAR did not bind to P300.

Conclusions:

  • Panaxytriol facilitates PXR recruitment to SRC-1 and P300, promoting binding to DNA response elements (ER-6/DR-3) and upregulating CYP3A4 expression.
  • An interactive regulatory mechanism between PXR and CAR in response to panaxytriol was identified.