Portulaca oleracea L. Extract Regulates Hepatic Cholesterol Metabolism via the AMPK/MicroRNA-33/34a Pathway in Rats Fed a High-Cholesterol Diet
- 주제(키워드) Portulaca oleracea L , cardiovascular disease , cholesterol metabolism , AMPK , microRNA
- 주제(기타) Nutrition & Dietetics
- 설명문(일반) [Jang, Sojeong; Lee, Mak-Soon; Kim, Yangha] Ewha Womans Univ, Dept Nutr Sci & Food Management, Seoul 03760, South Korea; [Jang, Sojeong; Kim, Yangha] Ewha Womans Univ, Dept Nutr Sci & Food Management, Grad Program Syst Hlth Sci & Engn, Seoul 03760, South Korea; [Kang, Sun-A; Kim, Chong-Tai] EastHill Corp, R&D Ctr, Suwon 16642, South Korea
- 등재 SCIE, SCOPUS
- OA유형 gold, Green Published
- 발행기관 MDPI
- 발행년도 2022
- URI http://www.dcollection.net/handler/ewha/000000194465
- 본문언어 영어
- Published As https://doi.org/10.3390/nu14163330
- PubMed https://pubmed.ncbi.nlm.nih.gov/36014836
초록/요약
This study examined the effect of extruded Portulaca oleracea L. extract (PE) in rats fed a high-cholesterol diet through the AMP-activated protein kinase (AMPK) and microRNA (miR)-33/34a pathway. Sprague-Dawley rats were randomized into three groups and fed either a standard diet (SD), a high-cholesterol diet containing 1% cholesterol and 0.5% cholic acid (HC), or an HC diet containing 0.8% PE for 4 weeks. PE supplementation improved serum, liver, and fecal lipid profiles. PE upregulated the expression of genes involved in cholesterol efflux and bile acids' synthesis such as liver X receptor alpha (LXR alpha), ATP-binding cassette subfamily G5/G8 (ABCG5/8), and cholesterol 7 alpha-hydroxylase (CYP7A1), and downregulated farnesoid X receptor (FXR) in the liver. In addition, hepatic gene expression levels of apolipoprotein A-l (apoA-1), paraoxonase 1 (PON1), ATP-binding cassette subfamily A1/G1 (ABCA1/G1), lecithin-cholesterol acyltransferase (LCAT), and scavenger receptor class B type 1 (SR-B1), which are related to serum high-density lipoprotein cholesterol metabolism, were upregulated by PE. Furthermore, hepatic AMPK activity in the PE group was higher than in the HC group, and miR-33/34a expression levels were suppressed. These results suggest that PE improves the cholesterol metabolism by modulating AMPK activation and miR-33/34a expression in the liver.
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