Abstract
Black elderberry (Sambucus Nigar) with high polyphenol content has been reported to have a hypolipidemic effect, but its underlying mechanisms have not been well characterized. In the present study, we investigated the effects of polyphenol-rich black elderberry (BEE) on oxidative stress and hepatic lipid metabolism. The total antioxidant activity of BEE was evaluated. The expression of genes for lipid metabolism was measured in 50 or 100 μg/mL of BEE-treated HepG2 cells. The mRNA and protein levels of genes for cholesterol metabolisms, i.e., sterol regulatory element-binding protein 2, 3-hydroxy-3-methylglutaryl coenzyme A reductase, and low-density lipoprotein receptor, were decreased by BEE. There was marked induction of genes for high-density lipoprotein metabolism, i.e., scavenger receptor class B type 1and ATP-binding cassette (ABC) transporter A1 in BEE-treated cells. The expression of canalicular efflux transporter for hepatic cholesterol and bile acids, such as ABCG5/G8 and ABCB11, was significantly increased by BEE treatment. There was no alteration of the lipogenic genes, whereas BEE significantly decreased the expression of genes for fatty acid oxidation. BEE significantly altered the expression of histone deacetylase and sirtuins. These data suggest that the hypocholesterolemic effects of BEE may be attributed to the alteration of genes for hepatic cholesterol synthesis and flux.
Highlights
Cardiovascular disease (CVD) is one of the leading causes of death worldwide [1]
Mounting evidence supports the existence of transintestinal cholesterol excretion (TICE), and hepatobiliary secretion mediated by reverse cholesterol transport (RCT) via High-density lipoprotein (HDL) is not the only route to eliminate excess cholesterol [7,8,9]
The total antioxidant capacity of black elderberry extract (BEE) was examined by measuring DPPH and ABTS radical scavenging activity and reducing power
Summary
Cardiovascular disease (CVD) is one of the leading causes of death worldwide [1]. The risk factors of CVD are obesity, hypertension, hyperglycemia, chronic low-grade inflammation, oxidative stress, and dyslipidemia [2]. High-density lipoprotein (HDL)-driven reverse cholesterol transport (RCT) mediated by the liver is considered the only route for cholesterol disposal in the body. Mounting evidence supports the existence of transintestinal cholesterol excretion (TICE), and hepatobiliary secretion mediated by RCT via HDL is not the only route to eliminate excess cholesterol [7,8,9]. This paradigm suggests that the underestimated role of the intestine in the classical concepts of cholesterol elimination requires modification and that TICE stimulation can be an effective target for the prevention of CVD [7].
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