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The Cholesterol-Lowering Effect of Capsella Bursa-Pastoris Is Mediated via SREBP2 and HNF-1α-Regulated PCSK9 Inhibition in Obese Mice and HepG2 Cells.

Authors
  • Hwang, Jin-Taek1, 2
  • Choi, Eunji3
  • Choi, Hyo-Kyoung1
  • Park, Jae-Ho1
  • Chung, Min-Yu1
  • 1 Korea Food Research Institute, Wanju-gun, Jeollabuk-do 55365, Korea. , (North Korea)
  • 2 Department of Food Biotechnology, Korea University of Science & Technology, Daejeon 34113, Korea. , (North Korea)
  • 3 Department of Food and Nutrition, Sookmyung Women's University, Seoul 04524, Korea. , (North Korea)
Type
Published Article
Journal
Foods
Publisher
MDPI AG
Publication Date
Feb 12, 2021
Volume
10
Issue
2
Identifiers
DOI: 10.3390/foods10020408
PMID: 33673187
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

The objective of the present study was to investigate the mechanism by which capsella bursa-pastoris ethanol extract (CBE), containing 17.5 milligrams of icaritin per kilogram of the extract, and icaritin, mediate hypocholesterolemic activity via the low-density lipoprotein receptor (LDLR) and pro-protein convertase subtilisin/kexin type 9 (PCSK9) in obese mice and HepG2 cells. CBE significantly attenuated serum total and LDL cholesterol levels in obese mice, which was associated with significantly decreased PCSK9 gene expression. HepG2 cells were cultured using delipidated serum (DLPS), and CBE significantly reduced PCSK9 and maintained the LDLR level. CBE co-treatment with rosuvastatin attenuated statin-mediated PCSK9 expression, and further increased LDLR. The icaritin contained in CBE decreased intracellular PCSK9 and LDLR levels by suppressing transcription factors SREBP2 and HNF-1α. Icaritin also significantly suppressed the extracellular PCSK9 level, which likely contributed to post-translational stabilization of LDLR in the HepG2 cells. PCSK9 inhibition by CBE is actively attributed to icaritin, and the use of CBE and icaritin could be an alternative therapeutic approach in the treatment of hypercholesterolemia.

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