Open AccessQuercetin‐3‐glucoside increases low‐density lipoprotein receptor (LDLR) expression, attenuates proprotein convertase subtilisin/kexin 9 (PCSK9) secretion, and stimulates LDL uptake by Huh7 human hepatocytes in culture
Author(s) -
Mbikay Majambu,
Sirois Francine,
Simoes Sonia,
Mayne Janice,
Chrétien Michel
Publication year - 2014
Publication title -
febs open bio
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.718
H-Index - 31
ISSN - 2211-5463
DOI - 10.1016/j.fob.2014.08.003
Subject(s) - pcsk9 , kexin , ldl receptor , proprotein convertase , chemistry , secretion , low density lipoprotein , endocrinology , medicine , lipoprotein , quercetin , cholesterol , biochemistry , biology , antioxidant
Low‐density lipoprotein receptor (LDLR) mediates hepatic clearance of plasma cholesterol; proprotein convertase subtilisin/kexin 9 (PCSK9) opposes this clearance by promoting LDLR degradation. The plant flavonoid quercetin‐3‐β‐ d ‐glucoside (Q3G) has been shown to reduce hypercholesterolemia in experimental animals. Here, we examined how it affects LDLR and PCSK9 expression as well as LDL uptake by human Huh7 hepatocytes. At low micromolar concentrations, Q3G increased LDLR expression, reduced PCSK9 secretion, and stimulated LDL uptake. It also diminished intracellular sortilin, a sorting receptor known to facilitate PCSK9 secretion. Thus, as an LDLR inducer and a PCSK9 anti‐secretagogue, Q3G may represent an effective anti‐cholesterolemic agent.