Abstract
ABSTRACT We examined the effects of Lithospermum erythrorhizon Sieb. et Zucc. (LE) on cholesterol metabolism in vitro. The ethanolic LE extract (ELE) had total polyphenolic and flavonoid contents of 353 ± 7 and 285 ± 51 mg/dL, respectively. The ELE inhibited Cu2+-mediated LDL oxidation at <400 µg/mL. In HepG2 cells treated with 400 µg/mL ELE, the expression of 3-hydroxy-3-methyl-glutaryl-CoA reductase decreased markedly (45%; P < 0.05), whereas that of the LDL receptor increased (230%; P < 0.05). The protein levels of both were altered similarly. The ELE also increased membrane-bound and cell-associated LDL particles, possibly via upregulation of the LDL receptor. In hepatocytes, 400 µg/mL ELE affected surrogate markers of HDL and LDL synthesis: significant expression of apolipoprotein A-I was induced (20%; P < 0.05), whereas that of apoB was suppressed (30%; P < 0.05). In conclusion, ELE may improve cellular cholesterol metabolism by inhibiting cholesterol biosynthesis and apoB production, accelerating plasma LDL uptake and reducing LDL oxidation. PRACTICAL APPLICATIONS Hypercholesterolemia is a major risk factor for coronary heart disease (CHD), which is the leading cause of mortality in patients with metabolic syndrome. Consequently, therapeutic interventions that prevent or treat metabolic disorders would markedly reduce metabolic syndrome-related death. Lipid-lowering drugs are effective at inhibiting hyperlipidemia, but have undesirable side effects and tolerance issues with long-term intake. Therefore, it is necessary for patients to undergo dietary modification using functional foods, including phytochemicals that have both nutritional and medicinal benefits, to prevent and attenuate hyperlipidemia. This study investigated the anti-atherogenic effects of an ethanolic Lithospermum erythrorhizon extract (ELE) in vitro. The results showed that the ELE inhibited low-density lipoprotein (LDL) oxidation, apoB production and cholesterol synthesis and induced LDL uptake. These results suggest that the ELE protects against atherogenesis and may help to prevent CHD.
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