Monica Deiana


Department of Biomedical Sciencesmonica deiana

Telephone: +39-070-6754126

Fax: +39-070-6754032


Personal webpage: here

Main areas of expertise: Oxidants, antioxidants and redox status modulation in pathophysiology


Oxidative stress and its modulation by antioxidant compounds and their metabolites

The research group of the Unit of Experimental Pathology, coordinated by Dr. Deiana, focuses mainly on oxidative stress and related diseases, and its modulation by antioxidant compounds and their metabolites. Suggestions that oxidative stress plays a role in human diseases have led to the proposal that health might be improved by increased dietary intake of antioxidants. Mediterranean–style diet is rich in plant-derived antioxidants, such as phenolic compounds and thiols. In the last years, the research group has evaluated the biopotency of dietary antioxidant factors, using various experimental models, from the simplest in vitro systems to the more complex studies on cell cultures and in vivo models. Currently major interest is centered on the toxicity of lipid oxidation products in relation to the inflammatory process and cell death that characterize inflammatory bowel diseases and atherosclerosis, and the modulatory activity of antioxidant compounds. The protective role of antioxidants and their metabolites is investigated as capacity of counteracting the oxidative damage, working as direct antioxidants, that scavenge excessive damaging free radicals, and as capacity to modulate cellular redox status, through the interaction with intracellular signaling cascades involved in the cellular response to oxidative injury.

Key publications:

  1. Serreli G, Melis MP, Corona G, Deiana M (2019). Modulation of LPS-induced nitric oxide production in intestinal cells by hydroxytyrosol and tyrosol metabolites: Insight into the mechanism of action. Food and Chemical Toxicology 125: 520-527
  2. Deiana M, Serra G, Corona G (2018). Modulation of intestinal epithelium homeostasis by extra virgin olive oil phenolic compounds. Food & Function 9: 4085-4099
  3. Serra G, Incani A, Serreli G, Porru L, Melis MP, Tuberoso CIG,, Rossin D, Biasi F, Deiana M (2018). Olive oil polyphenols reduce oxysterols -induced redox imbalance and pro-inflammatory response in intestinal cells. Redox Biology 17: 348-354
  4. Deiana M, Calfapietra S, Incani A, Atzeri A, Rossin D, Loi R, Sottero B, Iaia N, Poli G, Biasi F (2017). Derangement of intestinal epithelial cell monolayer by dietary cholesterol oxidation products. Free Radical Biology & Medicine 113: 539-550
  5. Serra G, Deiana M, Spencer JPE, Corona G (2017). Olive Oil Phenolics Prevent Oxysterol-Induced Pro-Inflammatory Cytokine Secretion and ROS Production in Human PBMCs, Through Modulation of p38 and JNK Pathways. Molecular Nutrition & Food Research 61, 1700283
  6. Incani A, Serra G, Atzeri A, Melis MP, Serreli G, Bandino G, Sedda P, Campus M, Tuberoso CIG, Deiana M (2016) Extra virgin olive oil phenolic extracts counteract the pro-oxidant effect of dietary oxidized lipids in human intestinal cells. Food and Chemical Toxicology 90: 171-180
  7. Atzeri A, Lucas R, Incani A, Peñalver P, Zafra-Gómez A, Melis MP, Pizzala R, Morales JC, Deiana M (2016) Hydroxytyrosol and tyrosol sulfate metabolites protect against the oxidized cholesterol pro-oxidant effect in Caco-2 human enterocyte-like cells. Food & Function 7: 337-346
  8. Guina T, Deiana M, Calfapietra S, Cabboi B, Maina M, Tuberoso CI, Leonarduzzi G, Gamba P, Gargiulo S, Testa G, Poli G, Biasi F (2015) The role of p38 MAPK in the induction of intestinal inflammation by dietary oxysterols: modulation by wine phenolics. Food & Function 6: 1218-1228
  9. Biasi F, Deiana M, Guina T, Gamba P, Leonarduzzi G, Poli G (2014) Wine consumption and intestinal redox homeostasis. Redox Biology 2: 795-802
  10. Biasi F, Guina T, Maina M, Cabboi B, Deiana M, Tuberoso CI, Calfapietra S, Chiarpotto E, Sottero B, Gamba P, Gargiulo S, Brunetto V, Testa G, Dessì MA, Poli G, Leonarduzzi G (2013) Phenolic compounds present in Sardinian wine extracts protect against the production of inflammatory cytokines induced by oxysterols in CaCo-2 human enterocyte-like cells. Biochemical Pharmacology 86: 138–145
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