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논문 기본 정보

자료유형
학술저널
저자정보
Kim Hyo-Jin (Personalized Diet Research Group, Korea Food Research Institute, Wanju 55365, Republic of KoreaDepartment of Food Biotechnology, University of Science) Park Seon Kyeong (Personalized Diet Research Group, Korea Food Research Institute, Wanju 55365, Republic of Korea) Park Soo Hyun (Personalized Diet Research Group, Korea Food Research Institute, Wanju 55365, Republic of Korea) Lee Yu Geon (Personalized Diet Research Group, Korea Food Research Institute, Wanju 55365, Republic of Korea) Park Jae-Ho (Personalized Diet Research Group, Korea Food Research Institute, Wanju 55365, Republic of Korea) Hwang Jin-Taek (Personalized Diet Research Group, Korea Food Research Institute, Wanju 55365, Republic of Korea) Chung Min-Yu (Department of Food and Nutrition, Gangseo University, Seoul 07661, Republic of Korea)
저널정보
한국미생물생명공학회 Journal of Microbiology and Biotechnology Journal of Microbiology and Biotechnology Vol.34 No.2
발행연도
2024.2
수록면
425 - 435 (11page)
DOI
10.4014/jmb.2306.06049

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Schisandra chinensis extract (SCE) protects against hypocholesterolemia by inhibiting proprotein convertase subtilisin/kexin 9 (PCSK9) protein stabilization. We hypothesized that the hypocholesterolemic activity of SCE can be attributable to upregulation of the PCSK9 inhibition-associated low-density lipoprotein receptor (LDLR). Male mice were fed a low-fat diet or a Western diet (WD) containing SCE at 1% for 12 weeks. WD increased final body weight and blood LDL cholesterol levels as well as alanine transaminase and aspartate aminotransferase expression. However, SCE supplementation significantly attenuated the increase in blood markers caused by WD. SCE also attenuated WDmediated increases in hepatic LDLR protein expression in the obese mice. In addition, SCE increased LDLR protein expression and attenuated cellular PCSK9 levels in HepG2 cells supplemented with delipidated serum (DLPS). Non-toxic concentrations of schisandrin A (SA), one of the active components of SCE, significantly increased LDLR expression and tended to decrease PCSK9 protein levels in DLPS-treated HepG2 cells. High levels of SA-mediated PCSK9 attenuation was not attributable to reduced PCSK9 gene expression, but was associated with free PCSK9 protein degradation in this cell model. Our findings show that PCSK9 secretion can be significantly reduced by SA treatment, contributing to reductions in free cholesterol levels.

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