In Vitro Chemopreventive Potential of Phlorotannins-Rich Extract from Brown Algae by Inhibition of Benzo[a]pyrene-Induced P2X7 Activation and Toxic Effects

Autor: Karim Hammad, Elodie Olivier, Romain Magny, Roxane Fagon, Sophie Fouyet, Emmanuel Roulland, Mélody Dutot, Patrice Rat
Přispěvatelé: Recherche & Développement, Yslab, 29000 Quimper, France, roxane.fagon@yslab.fr, Cibles Thérapeutiques et conception de médicaments (CiTCoM - UMR 8038), Institut de Chimie du CNRS (INC)-Centre National de la Recherche Scientifique (CNRS)-Université de Paris (UP)
Jazyk: angličtina
Rok vydání: 2021
Předmět:
Zdroj: Marine Drugs
Volume 19
Issue 1
Pages: 34
Marine drugs
Marine drugs, MDPI, 2021, 19 (1), pp.34. ⟨10.3390/md19010034⟩
Marine Drugs, Vol 19, Iss 34, p 34 (2021)
ISSN: 1660-3397
DOI: 10.3390/md19010034
Popis: International audience; Phlorotannins are polyphenols occurring exclusively in some species of brown algae, known for numerous biological activities, e.g., antioxidant, antiproliferative, antidiabetic, and antiallergic properties. Their effects on the response of human lung cells to benzo[a]pyrene (B[a]P) has not been characterized. Our objective was to in vitro evaluate the effects of a phlorotannin-rich extract obtained from the brown algae Ascophyllum nodosum and Fucus vesiculosus on B[a]P cytotoxic effects. The A549 cell line was incubated with B[a]P for 48 and 72 h in the presence or absence of the brown algae extract. Cytochrome P450 activity, activation of P2X7 receptor, F-actin disorganization, and loss of E-cadherin expression were assessed using microplate cytometry and fluorescence microscopy. Relative to control, incubation with the brown algae extract was associated with lower B[a]P-induced CYP1 activity, lower P2X7 receptor activation, and lower reactive oxygen species production. The brown algae extract inhibited the alterations of F-actin arrangement and the downregulation of E-cadherin expression. We identified a phlorotannins-rich extract that could be deeper investigated as a cancer chemopreventive agent to block B[a]P-mediated carcinogenesis.
Databáze: OpenAIRE