槲皮素-3-葡萄糖苷可增加低密度脂蛋白受体（LDLR）的表达，减弱前蛋白转化酶枯草溶菌素/kexin 9（PCSK9）的分泌，并刺激培养的Huh7人肝细胞摄取低密度脂蛋白。

Quercetin-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.

作者信息

Mbikay Majambu, Sirois Francine, Simoes Sonia, Mayne Janice, Chrétien Michel

机构信息

Chronic Disease Program, Ottawa Hospital Research Institute, Ottawa, Ontario, Canada ; Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, Ontario, Canada ; Laboratory of Functional Endoproteolysis, Clinical Research Institute of Montreal, Montreal, Quebec, Canada.

Chronic Disease Program, Ottawa Hospital Research Institute, Ottawa, Ontario, Canada ; Laboratory of Functional Endoproteolysis, Clinical Research Institute of Montreal, Montreal, Quebec, Canada.

出版信息

FEBS Open Bio. 2014 Sep 2;4:755-62. doi: 10.1016/j.fob.2014.08.003. eCollection 2014.

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.