Quercetin up-regulates LDL receptor expression in HepG2 cells

Jiyoung Moon, Seung Min Lee, Hyun Ju Do, Yoonsu Cho, Ji Hyung Chung, Min Jeong Shin

Research output: Contribution to journalArticlepeer-review

47 Citations (Scopus)


Quercetin, an abundant flavonol found in fruits and vegetable, has been implicated in lowering the risk of cardiovascular disease that is often associated with high plasma levels of low density lipoprotein (LDL) cholesterol. Here we investigated whether quercetin could modulate the expression of LDL receptors (LDLR) in HepG2 cells and the possible underlying mechanisms to exert quercetin's effects. We found that quercetin was able to induce LDLR expression with at least a 75 μ m concentration, which was accompanied by an increase in nuclear sterol regulatory element binding protein 2 (SREBP2). This effect was mediated by activation of c-jun-N-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK) signalling pathways as implicated by experiments using chemical inhibitors of each pathway. When cells were challenged with protein synthesis inhibitors in quercetin-activated LDLR transcription, LDL mRNA levels were not significantly affected by cycloheximide but puromycin abolished quercetin-induced LDLR transcription. Taken together, we conclude that quercetin can initiate LDLR transcription by enhancing SREBP2 processing, but new protein synthesis might be necessary to exert a maximum effect of quercetin in the up-regulation of the LDLR gene. Our findings demonstrate that quercetin strongly up-regulated LDLR gene expression, which might elicit hypolipidemic effects by increasing the clearance of circulating LDL cholesterol levels from the blood.

Original languageEnglish
Pages (from-to)1688-1694
Number of pages7
JournalPhytotherapy Research
Issue number11
Publication statusPublished - 2012 Nov


  • ERK
  • JNK
  • LDLR
  • SREBP2
  • quercetin

ASJC Scopus subject areas

  • Pharmacology


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