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RESEARCH PRODUCT
Sources, Chemistry, and Biological Potential of Ellagitannins and Ellagic Acid Derivatives
Predrag PutnikDanijela Bursać KovačevićVoster MuchenjeJosé M. LorenzoPaulo E.s. MunekataFrancisco J. Barbasubject
chemistry.chemical_classificationMAPK/ERK pathway0303 health sciences030309 nutrition & dieteticsNeurotoxicityPeroxisome proliferator-activated receptor04 agricultural and veterinary sciencesPharmacologymedicine.disease040401 food scienceUrolithin03 medical and health sciencesIκBαchemistry.chemical_compound0404 agricultural biotechnologychemistryPolyphenolmedicinePunicalaginEllagic aciddescription
Abstract The consumption of polyphenols is considered an important part of a healthy life style and is related to reducing the risk for diseases. Ellagitanins (e.g., vescalagin, punicalagin, and castalagin) and ellagic acid and its derived compounds (e.g., urolithin) have been receiving attention in recent years as bioactive substances. This class of phenolic substances can be found in berries, pomegranates, walnuts, almonds, and other plant material that is consumed as traditional medicine to treat inflammatory diseases. Human gut microbiota are considered to play an important role in the bioactivity of ellagic acid derivative activity due to the production of urolithin and its antiinflammatory potential. Many studies have been clarifying, at least in part, the mechanism involved in the bioactivity of ellagitannins and ellagic acid and its derivatives in a number of areas: attenuation of the deleterious effect of oxidized low-density lipoprotein-induced endothelial dysfunction by modulating miR-27 expression and the ERK/PPAR-γ pathway on cardiovascular protection; inhibition of α-glucosidase and lipogenic gene expression in diabetes; inhibition of MMP-9 secretion and expression in malaria; mediation of estrogen receptor α-dependent gene expression and prevention of hepatocyte growth factor and phosphatidylinositol 3-kinase/AKT activation in cancer cells; inhibition of β-amyloid fibrillation and protection against neurotoxicity and paralysis in Alzheimer's disease; inhibition of lipopolysaccharide-induced inflammation macrophages by inhibiting the IκBα and p65 phosphorylation involved in NF-κB activation in inflammatory diseases.
year | journal | country | edition | language |
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2019-01-01 |