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Effects of phenolic compounds in blueberries and muscadine grapes on HepG2 cell viability and apoptosis
Affiliation:1. Department of Food Science and Technology, The University of Georgia, Athens, GA 30602-7610, United States;2. Department of Foods and Nutrition, The University of Georgia, Athens, GA 30602-3622, United States;3. Department of Horticulture, The University of Georgia, Tifton, GA 31793, United States
Abstract:Although blueberries and muscadine grapes have high contents of polyphenols, few studies have been conducted to assess their potential effects on cancer cells. The objective of this study was to systematically evaluate the effects of different fractions of phenolic compounds in blueberries and muscadine grapes on HepG2 liver cancer cell viability and apoptosis. Three cultivars of blueberries (‘Briteblue’, ‘Tifblue’ and ‘Powderblue’) and four cultivars of muscadine grapes (‘Carlos’, ‘Ison’, ‘Noble’, and ‘Supreme’) were assessed in this study. Polyphenols were extracted and further separated into phenolic acids, tannins, flavonols, and anthocyanins using a HLB cartridge and LH-20 column. The major compounds of different fractions were characterized. The phenolic acid fractions of muscadine grapes and blueberries showed a 50% inhibition of HepG2 cell population growth at the level of 1–2 mg/mL. The greatest inhibitory effects were observed from the anthocyanin fractions with 50% inhibitions of cancer cell population growth at concentrations of 70–150 and 100–300 μg/mL in blueberries and muscadine grapes, respectively. The flavonol and tannin fractions showed intermediate activities. In addition, DNA fragmentation was measured by using a Cell Death Detection ELISA kit to assess the induction of apoptosis. The anthocyanin fraction resulted in a two- to fourfold increase in DNA fragmentation compared to control in both muscadine grapes and blueberries. These findings of inhibition of cancer cell growth and induction of apoptosis suggest that blueberries and muscadine grapes may contribute to reduction in liver cancer risk.
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