Punicalagin protects human retinal pigment epithelium cells from ultraviolet radiation-induced oxidative damage by activating nrf2/ho-1 signaling pathway and reducing apoptosis

Giuseppe Tringali, Maria Elisabetta Clementi, Francesca Sciandra

Risultato della ricerca: Contributo in rivistaArticolo in rivistapeer review

3 Citazioni (Scopus)

Abstract

The oxidative damage of the retinal pigment epithelium (RPE) is the early event that underlies the pathogenesis of maculopathies. Numerous studies have shown that punicalagin (PUN), a polyphenol present in pomegranate, can protect several cell types from oxidative stress. Our study aims to establish if PUN protects RPE from UV radiation-induced oxidative damage. We used an experimental model which involves the use of a human-RPE cell line (ARPE-19) exposed to UV-A radiation for 1, 3, and 5 hours. ARPE-19 cells were pre-treated with PUN (24 h) followed by UV-A irradiation; controls were treated identically, except for UV-A. Effects of pre-treatment with PUN on cell viability, intracellular reactive oxygen species ROS levels, modulation of Nrf2 and its antioxidant target genes, and finally apoptosis were examined. We found that pre-treatment with PUN: (1) antagonized the decrease in cell viability and reduced high levels of ROS associated with UV-A-induced oxidative stress; (2) activated Nrf2 signaling pathway by promoting Nrf2 nuclear translocation and upregulating its downstream antioxidant target genes (HO-1 and NQO1); (3) induced an anti-apoptotic effect by decreasing Bax/Bcl-2 ratio. These findings provide the first evidence that PUN can prevent UV-A-induced oxidative damage in RPE, offering itself as a possible antioxidant agent capable of contrasting degenerative eye diseases.
Lingua originaleEnglish
pagine (da-a)N/A-N/A
Numero di pagine13
RivistaAntioxidants
Volume9
DOI
Stato di pubblicazionePubblicato - 2020

Keywords

  • Apoptosis
  • ARPE-19 (human-RPE cell line)
  • Punicalagin
  • NADPH quinone dehydrogenase-1 (NQO1)
  • Nuclear factor erythroid 2-related factor (Nrf2)
  • Heme oxygenase-1 (HO-1)

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