Abstract

Purpose Blueberry contains bioactive compounds which are beneficial to organisms, such as phenolics and flavonoids. The purpose of this paper is to evaluate the potential protective effects of blueberry extracts (BE) on H2O2-induced HepG2 cells. Design/methodology/approach Cell protection was evaluated via the survivals of the cell. Reactive oxygen species (ROS) level, antioxidant enzyme and malondialdehyde (MDA) were detected. Western blot was carried out to analysis protein which was related to the cell apoptosis pathway. Changes in morphology including: cell total apoptosis/necrosis and G0/G1 cycle arresting were also concomitant. Findings The levels of ROS and malondialdehyde (MDA) reduced after the BE treatment while the contents of superoxide dismutase, and glutathione peroxidase (GSH-Px) increased in HepG2 cells induced by H2O2. Furthermore, mechanistic studies indicated that BE regulated the activation of mitochondrial apoptosis signal-regulating (Bcl-2, Bax). Qu was used as a positive control group. All these results demonstrated that the BE have a potential against oxidative stress in vitro. Originality/value Few studies have focused on the bioactivities of blueberry on oxidative stress. Taken together, the results confirm that polyphenol-enriched BE have the ability to protect against oxidative stress in cells. It has a great potential as a functional food ingredient to health benefits. Furthermore, this work showed the value of using simple biological models to screen for compounds that are of interest for food and pharmacological industry.

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