ABSTRACT
Over the past two decades, extensive studies have revealed that inflammation represents a major risk factor for various human diseases. Chronic inflammatory responses predispose to pathological progression of chronic illnesses featured with penetration of inflammatory cells, dysregulation of cellular signaling, excessive generation of cytokines, and loss of barrier function. Hence, the suppression of inflammation has the potential to delay, prevent, and to treat chronic diseases. Flavonoids, which are widely distributed in humans daily diet, such as vegetables, fruits, tea and cocoa, among others, are considered as bioactive compounds with anti-inflammatory potential. Modification of flavonoids including hydroxylation, o-methylation, and glycosylation, can alter their metabolic features and affect mechanisms of inflammation. Structure–activity relationships among naturally occurred flavonoids hence provide us with a preliminary insight into their anti-inflammatory potential, not only attributing to the antioxidant capacity, but also to modulate inflammatory mediators. The present review summarizes current knowledge and underlies mechanisms of anti-inflammatory activities of dietary flavonoids and their influences involved in the development of various inflammatory-related chronic diseases. In addition, the established structure–activity relationships of phenolic compounds in this review may give an insight for the screening of new anti-inflammatory agents from dietary materials.
Conflict of interest
None declared
Abbreviations
COX | = | Cyclooxygenase |
CXCL | = | Chemokine (C-X-C motif) ligand |
ERK | = | Extracellular signal-regulated kinase |
ICAM-1 | = | Intercellular adhesion molecule-1 |
IκB | = | Inhibitor of κB |
IKK | = | IκB kinase |
IL | = | Interleukin |
iNOS | = | Inducible nitric oxide synthase |
JAK | = | Janus tyrosine kinase |
JNK | = | c-Jun N-terminal kinase |
LPS | = | Lipopolysaccharide |
LOX | = | Lipoxygenase |
MAPK | = | Mitogen-activated protein kinase |
NF-κB | = | Nuclear factor-κB |
NO | = | Nitric oxide |
NOS | = | Nitric oxide synthase |
PI3K | = | Phosphatidylinositol 3-kinase |
PKC | = | phospho kinase C |
PLA2 | = | Phospholipase A2 |
PGE2 | = | Prostaglandin E2 |
ROS | = | Reactive oxygen species |
STAT | = | Signal transducers and activators of transcription |
TNF | = | Tumor necrosis factor |
VCAM-1 | = | vascular cell adhension molecule-1 |