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Olive oil polyphenols reduce oxysterols -induced redox imbalance and pro-inflammatory response in intestinal cells

Serra G, Incani A, Serreli G, Porru L, Melis MP, Tuberoso CIG, Rossin D, Biasi F, Deiana M

Redox biology · 85 citas

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Cómo se estudió

Diseño
Estudio in vitro o de mecanismos (clasificado por nuestro filtro de IA)
Estudiado en
Células o muestras de laboratorio
Resultado principal
Solo mecanismos

Quién lo pagó

Financiación
Financiación independiente
Universidad u hospital
Rochester Academy of Science
Gobierno
Regione Autonoma della Sardegna
Subvenciones
Regione Autonoma della Sardegna (LR7- CRP-25300)

Según 2 financiadores declarados y la declaración de financiación del texto completo.

Publicación

Publicado
2018-05-16 · Redox Biol · vol. 17 · págs. 348–354
Editorial
Elsevier BV
Citado
102 citas · más que el 99% de estudios similares · 12.8× el promedio de su campo
Impacto
Entre el 10 % más citado de su campo
Referencias
69 trabajos
Acceso
Acceso abierto (revista) · CC-BY
Áreas de investigación
Cholesterol and Lipid Metabolism · Ginger and Zingiberaceae research · Garlic and Onion Studies
Palabras clave
Oxysterol, Chemistry, Antioxidant, Enterocyte, p38 mitogen-activated protein kinases, Caco-2, Biochemistry, MAPK/ERK pathway, Oxidative stress, Inflammation, Phosphorylation, Cholesterol, Pharmacology, Cell biology, Biology, Cell, Immunology, Small intestine
MeSH
intestines, intestinal mucosa, caco-2 cells, humans, inflammation, nitric oxide, reactive oxygen species, nf-kappa b, interleukin-8, interleukin-6, antioxidants, signal transduction, oxidation-reduction, oxidative stress, polyphenols, olive oil, oxysterols

9 autores

  • Gessica Serra🇬🇧University of Reading
  • Alessandra Incani🇮🇹University of Cagliari
  • Gabriele Serreli🇮🇹University of Cagliari
  • Laura Porru🇮🇹University of Cagliari
  • Maria Paola Melis🇮🇹University of Cagliari
  • Carlo Ignazio Giovanni Tuberoso🇮🇹University of Cagliari
  • Daniela Rossin🇮🇹University of Turin
  • Fiorella Biasi🇮🇹University of Turin
  • Monica Deiana🇮🇹 · autor de correspondenciaUniversity of Cagliari

Resumen

El texto original del estudio, en el idioma en que se publicó.

Dietary habits may strongly influence intestinal homeostasis. Oxysterols, the oxidized products of cholesterol present in cholesterol-containing foodstuffs, have been shown to exert pro-oxidant and pro-inflammatory effects, altering intestinal epithelial layer and thus contributing to the pathogenesis of human inflammatory bowel diseases and colon cancer. Extra virgin olive oil polyphenols possess antioxidant and anti-inflammatory properties, and concentrate in the intestinal lumen, where may help in preventing intestinal diseases. In the present study we evaluated the ability of an extra virgin olive oil phenolic extract to counteract the pro-oxidant and pro-inflammatory action of a representative mixture of dietary oxysterols in the human colon adenocarcinoma cell line (Caco-2) undergoing full differentiation into enterocyte-like cells. Oxysterols treatment significantly altered differentiated Caco-2 cells redox status, leading to oxidant species production and a decrease of GSH levels, after 1 h exposure, followed by an increase of cytokines production, IL-6 and IL-8, after 24 h. Oxysterol cell treatment also induced after 48 h an increase of NO release, due to the induction of iNOS. Pretreatment with the phenolic extract counteracted oxysterols effects, at least in part by modulating one of the main pathways activated in the cellular response to the action of oxysterols, the MAPK-NF-kB pathway. We demonstrated the ability of the phenolic extract to directly modulate p38 and JNK1/2 phosphorylation and activation of NF-kB, following its inhibitor IkB phosphorylation. The phenolic extract also inhibited iNOS induction, keeping NO concentration at the control level. Our results suggest a protective effect at intestinal level of extra virgin olive oil polyphenols, able to prevent or limit redox unbalance and the onset and progression of chronic intestinal inflammation.

Resumen vía Europe PMC. Los derechos de autor siguen siendo de los autores o la editorial (CC BY).

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