Abstract
Hypercholesterolemia is one of the modifiable and primary risk factors for cardiovascular diseases (CVD). Emerging evidence suggests the stimulation of transintestinal cholesterol excretion (TICE), the nonbiliary cholesterol excretion, using natural products can be an effective way to reduce CVD. Bilberry (Vaccinium myrtillus L.) has been reported to have cardioprotective effects by ameliorating oxidative stress, inflammation, and dyslipidemia. However, the role of bilberry in intestinal cholesterol metabolism is not well understood. To examine the effects of bilberry in intestinal cholesterol metabolism, we measured the genes for cholesterol flux and de novo synthesis in anthocyanin-rich bilberry extract (BE)-treated Caco-2 cells. BE significantly decreased the genes for cholesterol absorption, i.e., Niemann-Pick C1 Like 1 and ATP-binding cassette transporter A1 (ABCA1). In contrast, BE significantly upregulated ABCG8, the apical transporter for cholesterol. There was a significant induction of low-density lipoprotein receptors, with a concomitant increase in cellular uptake of cholesterol in BE-treated cells. The expression of genes for lipogenesis and sirtuins was altered by BE treatment. In the present study, BE altered the genes for cholesterol flux from basolateral to the apical membrane of enterocytes, potentially stimulating TICE. These results support the potential of BE in the prevention of hypercholesterolemia.
Highlights
Hyperlipidemia, including hypercholesterolemia and hypertriglyceridemia, is a modifiable risk factor for atherosclerosis and cardiovascular disease (CVD) [1]
We investigated the effects of bilberry extract (BE) in regulating genes involved in intestinal cholesterol metabolism using Caco-2 cells
Phenolics, and flavonoids in BE, the standardized bilberry extract to 25% anthocyanins, exerted 237.9 ± 17.1 mg cyanidin-3-glucoside equivalents (CGE)/g, 338.5 ± 28.0 mg gallic acid equivalents (GAE)/g, and 735.4 ± 18.2 mg quercetin equivalents (QE)/g, respectively (Table 3)
Summary
Hyperlipidemia, including hypercholesterolemia and hypertriglyceridemia, is a modifiable risk factor for atherosclerosis and cardiovascular disease (CVD) [1]. The liver, a central site for cholesterol homeostasis, plays a primary role in de novo biosynthesis, assembly and uptake of cholesterol, and conversion of cholesterol to bile acids for biliary secretion. The reverse cholesterol transport pathway driven by high-density lipoprotein has been recognized as the only route to remove cholesterol from the body. In this hepatobiliary cholesterol excretion pathway, the cholesterol is secreted to bile from the liver for subsequent excretion as a fecal neutral sterol [4,5,6]. Enterocytes can directly take up circulating lipoprotein-derived cholesterol from plasma for subsequent disposal into the intestinal lumen in this alternative pathway for cholesterol elimination [10,11].
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