Abstract
Inflammation involving the innate and adaptive immune systems is a normal response to infection; however, when allowed to continue unchecked, inflammation may result in several pathologies. Natural molecules with antioxidant properties can target the key players of inflammation and exert beneficial health effects. In this study, human normal bronchial (Beas-2B) and prostate (HPrEpiC) epithelial cell lines were exposed to infectious stimulation and treated with phycocyanin (PC) and palmitoylethanolamide (PEA), with the aim of demonstrating the enhanced antioxidant and anti-inflammatory properties of the combination. The cotreatment protected from cytotoxicity and greatly abated both the production of radical oxygen species (ROS) and the transcription of several inflammatory cytokines. Oxidative stress and inflammation were curtailed by affecting three main pathways: (1) inhibition of cyclooxygenase-2 enzyme and consequent decrease of signaling generating ROS; (2) increased synthesis of glutathione and therefore strengthening of the natural antioxidant defenses of the cells; (3) decreased infection-driven mitochondrial respiratory burst which generates oxidative stress. Based on the mounting interest in using nutraceuticals as adjuvants in the clinical practice, the present study unveils new mechanisms of action and enhanced efficacy of PC and PEA, supporting the possible exploitation of this combination in human disorders.
Highlights
The goal of the inflammatory process is the full recovery to a state of good health and the return to conditions of homeostasis [1]
As PC exerts its anti-inflammatory activity through the inhibition of COX-2 enzymatic activity, we sought to confirm this property as well as explore the possible synergy with
The in vitro analysis of COX-2 activity revealed the inhibition exerted by both molecules
Summary
The goal of the inflammatory process is the full recovery to a state of good health and the return to conditions of homeostasis [1]. To recruit additional immune cells to the site of infection, inflammation triggers the secretion of various cytokines and chemokines by immune cells [2]. The activation of the nuclear transcription factor NF-κB, and the production of radical oxygen species (ROS) are the main mediators on which converge several inflammatory stimuli. NF-κB and ROS signaling are strictly linked and stimulate each other. Several signals such as inflammatory cytokines, LPS (bacterial lipopolysaccharide), viral particles and other mediators that activate TLRs (Toll-Like Receptors), known as pathogen-associated molecular patterns (PAMPS), converge on the TLR/NF-κB axis. The microbial and viral components, LPS and Poly(I:C) (TLR4 and TLR3 agonists, respectively), trigger
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