Abstract
This study investigated the protective effect and the molecular mechanism of piceatannol on hydrogen peroxide (H2O2)-induced retinal pigment epithelium cell (ARPE-19) damage. Piceatannol treatment significantly inhibited H2O2-induced RPE cell death and reactive oxygen species (ROS) generation by 64.4% and 75.0%, respectively. Results of flow cytometry showed that H2O2-induced ARPE-19 cells apoptosis was ameliorated by piceatannol supplementation, along with decreased relative protein expressions of Bax/Bcl-2, Cleave-Caspase-3, and Cleave-PARP. Moreover, piceatannol treatment induced NF-E2-related factor 2 (Nrf2) signaling activation, which was evidenced by increased transcription of anti-oxidant genes, glutamate-cysteine ligase catalytic subunit (GCLc), SOD, and HO-1. Knockdown of Nrf2 through targeted siRNA alleviated piceatannol-mediated HO-1 transcription, and significantly abolished piceatannol-mediated cytoprotection. LY294002 (PI3K inhibitor) dramatically blocked piceatannol-mediated increasing of Nrf2 nuclear translocation, HO-1 expression, and cytoprotective activity, indicating the involvement of PI3K/Akt pathway in the cytoprotective effect of piceatannol. The results from this suggest the potential of piceatannol in reducing the risk of age-related macular degeneration.
Highlights
Age-related macular degeneration (AMD) can cause irreversible vision loss which is a major threat for eye health in aging populations [1,2,3]
The results showed that piceatannol treatment had no significant adverse effect on retinal pigment epithelial (RPE) cells’
The PI3K/Akt signaling pathway played a vital role in piceatannol protection against H2 O2 -induced RPE cells oxidant damage
Summary
Age-related macular degeneration (AMD) can cause irreversible vision loss which is a major threat for eye health in aging populations [1,2,3]. AMD is characterized by the degeneration of the macular retinal pigment epithelial (RPE) cells. Excessive reactive oxygen species (ROS) is one of the major risk factors for AMD, which causes oxidation of key cellular components and severe damage to local retinal pigment epithelium (RPE) cells pathophysiologically. Clinical studies revealed that antioxidants and zinc-containing supplements could dramatically reduce AMD progression rate [4]. Reported that increased consumption of fruits and vegetables containing antioxidant nutrients and phytochemicals might provide some protection against AMD [5].
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