Dietary resveratrol increases the expression of hepatic 7α-hydroxylase and ameliorates hypercholesterolemia in high-fat fed C57BL/6J mice

Lipids Health Dis. 2012 May 20:11:56. doi: 10.1186/1476-511X-11-56.

Abstract

Background: Resveratrol (RSV), a naturally occurring polyphenolic stilbenoid, is known to possess potent anti-atherogenic properties; however, the effect of RSV on hypercholesterolemia is not fully understood. We hypothesized that RSV decreases blood cholesterol levels through the activation of cholesterol 7α-hydroxylase (CYP7A1)-mediated bile acid synthetic pathway pathways in vitro and in vivo.

Methods: In this study, we evaluated body weight, serum lipid concentrations, hepatic lipid content and the size of the bile acid pool in high-fat diet (HFD)-fed C57BL/6 J mice that were treated with RSV. In addition, we characterized the underlying mechanism of the effects of RSV in HepG2 hepatocytes by Western blot analysis.

Results: RSV (200 mg/kg per day) reduced body weight and liver weight gains, improved serum lipid parameters, reduced hepatic cholesterol accumulation and increased the bile acid pool size in mice fed an HFD for 8 wks. RSV significantly increased liver expression of CYP7A1 mRNA and protein and CYP7A1 enzyme activity. Furthermore, RSV treatment upregulated CYP7A1 expression and induced liver X receptor alpha (LXRα) activation in a time- and dose-dependent manner in HepG2 cells. In addition, the specific liver X receptor alpha (LXRα) inhibitor geranylgeranyl pyrophosphate (GGPP) inhibited the RSV-induced expression of CYP7A1 in HepG2 hepatocytes.

Conclusion: The beneficial effects of RSV on HFD-induced hypercholesterolemia are mediated through LXRα signaling pathways, suggesting a potential target for the prevention of dyslipidemia.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cholesterol 7-alpha-Hydroxylase / genetics
  • Cholesterol 7-alpha-Hydroxylase / metabolism*
  • Diet, High-Fat / adverse effects*
  • Dietary Supplements*
  • Hep G2 Cells
  • Humans
  • Hypercholesterolemia / drug therapy*
  • Hypercholesterolemia / etiology
  • Hypolipidemic Agents / administration & dosage*
  • Liver / enzymology*
  • Liver X Receptors
  • Mice
  • Mice, Inbred C57BL
  • Orphan Nuclear Receptors / metabolism
  • Resveratrol
  • Stilbenes / administration & dosage*
  • Transcription, Genetic
  • Transcriptional Activation

Substances

  • Hypolipidemic Agents
  • Liver X Receptors
  • NR1H3 protein, human
  • Nr1h3 protein, mouse
  • Orphan Nuclear Receptors
  • Stilbenes
  • Cholesterol 7-alpha-Hydroxylase
  • Cyp7a1 protein, mouse
  • Resveratrol