Abstract: This review offers a systematic understanding about how polyphenols target multiple
inflammatory components and lead to anti-inflammatory mechanisms. It provides a clear
understanding of the molecular mechanisms of action of phenolic compounds. Polyphenols regulate
immunity by interfering with immune cell regulation, proinflammatory cytokines’ synthesis, and
gene expression. They inactivate NF-κB (nuclear factor kappa-light-chain-enhancer of activated
B cells) and modulate mitogen-activated protein Kinase (MAPk) and arachidonic acids pathways.
Polyphenolic compounds inhibit phosphatidylinositide 3-kinases/protein kinase B (PI3K/AkT),
inhibitor of kappa kinase/c-Jun amino-terminal kinases (IKK/JNK), mammalian target of rapamycin
complex 1 (mTORC1) which is a protein complex that controls protein synthesis, and JAK/STAT.
They can suppress toll-like receptor (TLR) and pro-inflammatory genes’ expression. Their antioxidant
activity and ability to inhibit enzymes involved in the production of eicosanoids contribute as well to
their anti-inflammation properties. They inhibit certain enzymes involved in reactive oxygen species
ROS production like xanthine oxidase and NADPH oxidase (NOX) while they upregulate other
endogenous antioxidant enzymes like superoxide dismutase (SOD), catalase, and glutathione (GSH)
peroxidase (Px). Furthermore, they inhibit phospholipase A2 (PLA2), cyclooxygenase (COX) and
lipoxygenase (LOX) leading to a reduction in the production of prostaglandins (PGs) and leukotrienes
(LTs) and inflammation antagonism. The effects of these biologically active compounds on the
immune system are associated with extended health benefits for different chronic inflammatory
diseases. Studies of plant extracts and compounds show that polyphenols can play a beneficial role inprevention and the progress of chronic diseases related to inflammation such as diabetes, obesity,
neurodegeneration, cancers, and cardiovascular diseases, among other conditions.
Keywords: polyphenols; immune system; inflammation; molecular mechanisms; nuclear factor
kappa-light-chain-enhancer of activated B cells (NF-κB); arachidonic acid; mitogen-activated
protein Kinase (MAPK); cytokines; oxidative stress; reactive oxygen species (ROS); cyclooxygenase
(COX); nitric oxide synthase (NOS); lipoxygenase (LOX); superoxide dismutase (SOD); inhibitor
of kappa kinase (IKK); extra-cellular signal regulated kinases (ERK); cancer; anti-inflammation;
anti-tumorigenic; chronic inflammatory conditions; macrophages; T helper 1 (Th1); Th17; Treg
To read full article https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6266803/